Biological and Cognitive Psychology

Biological and Cognitive Psychology
Biological and Cognitive Psychology: Book Notes
Lecturer: Dr. Dennis van ‘t Ent and Dr. Richard Godijn
Tutor: Linda Bettelli
Literature: Physiology of behavior (13th edition)
ECT: 9
Biological and Cognitive Psychology: Summary
Chapter 1: Introduction
● Compare the roles of generalization and reduction in behavioral neuroscience
research.
○ End of 20th century: Many researchers believed that our brains are incapable
of change in adulthood → But actually, adult brains are flexible (or plastic)
and thus experience neural changes.
○ Neurons: Basic unit of our nervous system; communicate with other neurons
to convert information as neural networks which the brain can process.
■ Neurogenesis: The generation of new neurons in specific regions of
the adult brain. The hippocampus is typically associated with this.
○ 2 forms of explanation:
1. Generalization: Explanations as examples of general laws, which are
revealed through experiments.
2. Reduction: Explanations of complex phenomena in terms of simpler
ones.
○ Behavioral neuroscientists seek to explain behavior by studying the
physiological processes that control it.
● Summarize historical and contemporary contributions to behavioral neuroscience

from various scientific disciplines.
○ Contributions from the ancient world: Role of the Heart and the Brain
■ 1700 BCE: Surgical records of head injuries and the oldest surviving
descriptions of the brain, cerebrospinal fluid, and skull.
■ Ancient cultures (e.g. Indian, Chinese, Egyptians, Greeks, etc.)
believed that the heart was the “seat” of thoughts and emotions.
○ Contributions from philosophy: The mind-body question
■ Historical times questions: What role does the mind play in our
bodies? Does it control the nervous system?
■ Is it physical like the rest of the body or is it only a spirit that will
remain hidden?
■ In answering these questions, people followed 2 different approaches:

1. Dualism: A belief in the dual nature of reality → body and
mind are separate entities. The body is made of ordinary matter
but the mind is not.
2. Monism: A belief that everything in the universe consists of
matter and energy and the mind is a phenomenon produced by
the workings of the nervous system.
■ Contribution of Rene Descartes on the mind-body question

● He believed animals’ behavior was controlled by
environmental stimuli → like a machine.
● Some movements are voluntary, some are involuntary.
● Important: He believed that the mind controlled the
movements of the body, while the body supplied the mind
with information about what was happening in the
environment.
● He believed that the brain used pressurized fluid to control
behavior.
○ Contributions from Physiology: Electrical Communication in the Nervous
System
■ Physiologist Galvani disproved Descartes and found that electrically
stimulating a frog’s nerve contracted the muscle to which it was
attached.
■ Galvani’s experiment prompted others to study the nature of the
message transmitted by the nerve and the means by which muscles
contracted.
■ The doctrine of specific nerve energies: Physiologist Muller observed
that although all nerves carry the same basic message (an electrical
impulse), we perceive the messages of different nerves in different
ways.
● How can different sensations arise from the same basic
message? → nerves have different channels (the brain is
functionally divided: Some parts perform some functions, while
other parts perform others).
■ 1870: Physiologists Gustac and Hitzig applied weak electrical current

to the exposed surface of a dog’s brain and observed the effects of the
stimulation.
● Observation: A specific region of the brain (we now call it the
primary motor cortex) causes specific muscles to contract on
the opposite side of the body.
○ Contributions from anatomy: Structure of the nervous system

■ Pierre Flourens moved various parts of animals’ brains and observed
their behavior.
● This method is called experimental ablation.
■ → Paul Broca soon applied this method to the human brain.
● He investigated the brain of a man who had a stroke that
resulted in the loss of the ability to speak.
● This observation led him to see that the damage was on the
region on the left hemisphere which later became known as
Broca’s area.
■ Mid-19th century: Physiologist Jan Purkinje studied both the central
and peripheral nervous system → discovered Purkinje fibers (neurons
responsible for controlling contractions of the heart).
● Investigated structure of neurons in regions of the brain with a
microscope → discovered Purkinje cells in the cerebellum.
■ Late-19th century: Santiago Ramon y Cajal used the Golgi staining
technique to examine individual neurons of the brain.
○ Contemporary research contributions

■ Optogenetics → provided researchers with the ability to selectively
activate single neurons and observe changes in behavior, using light!
■ Treatments for psychological disorders (e.g. Parkinson’s disease)
■ Refined understandings of the structure and function of the brain.
■ The Society for Neuroscience (1969) is an organization of physicians
and scientists devoted to understanding the brain and nervous system.
● Members from all over the world → diversity.
● Describe the role of natural selection in the evolution of behavioral traits.

○ Functionalism: The principle that characteristics of living organisms perform
useful functions.
○ Natural selection: Those species that are most adapted to their environment
live on to pass on their genes to their offspring, the next generation →
characteristic more prevalent.
■ These adaptations’ functions allow the offspring to be better adapted
and thus behave in a certain way that will allow them to live on.
○ Artificial selection: Controlled by animal breeders.
○ Mutations: Accidental changes in the chromosomes of sperm or eggs that
result in a new organism because the structure and chemistry of the cell is
altered. Mostly physical mutations.
■ The effects of these physical alterations can be seen in the species’s
behavior.
■ Beneficial: Selective advantage to organisms.
■ No effect
■ Disadvantage
○ Evolution: The gradual change in structure and physiology of a plant or
animal as a result of natural selection.
■ The brain at birth has a number of neural circuits which can be
programmed.
■ Brains vary in size and number of neurons.
■ Neoteny: The prolongation of the brain’s maturation.
● Identify factors involved in the evolution of human brains.

○ To evolve means to develop gradually.
○ Evolution of color vision of humans helped them spot ripe fruit, prey, and
dangerous predators.
■ Their eyes are far enough from the ground to see long distances across
the plains.
○ Their linguistic abilities allowed them to combine collective knowledge →
pass information.
○ The evolution of these functions (e.g. color vision, motor control, language)
led to the evolution of a more complex primate brain.
○ Additional brain development occurs after birth with parental care.
● Outline reasons for the use of animals in behavioral neuroscience research.

○ Animals are used to improve understanding of the nervous system and develop
treatments for disease and injury.
○ They are used when it is not possible to conduct research with humans or
when computers cannot simulate the nervous system.
● Identify mechanisms for oversight of animal research.

○ The IACUC ( Institutional Animal Care and Use Committee) is responsible
for the local, state and federal regulations of animal research.
○ They review animal research proposals and protect the welfare of animals.
● Discuss ethical considerations in research with human participants.

○ Confidentiality: Inability to share information with others.
○ Benificence: The researchers/ scientists ar responsible for the welfare of the
participants.
○ Informed consent: The participants have the rights to know about the
experiment.
● Identify mechanisms for oversight of human research.

○ IRB (Institutional Review Board) is responsible for the ethical treatments on
humans.
■ Composed of community members, laypeople and experts to review
studies/experiments involving humans.
● Identify careers in behavioral neuroscience.

○ Researchers work in the fields of general neuroscience, behavioral
neuroscience and cognitive neuroscience.
○ Neurologists specialize in the nervous system.
○ Individuals pursuing careers in neuroscience work in academia or industry and

pursue graduate education.
● Describe effective learning strategies for studying behavioral neuroscience.

○ Active strategies are most effective.
○ Taking notes, practicing teaching, sharing information, few distractions,
planning, pneumonics.
Chapter 2: Structure and Functions of Cells of the Nervous System

● Contrast features of the central and peripheral nervous systems.
○ CNS contains the brain and spinal cord.
■ The CNS gets information from the outside world and transmits this
information to the brain.
○ PNS includes the nerves and most sensory organs outside the brain and spinal
cord.
■ The PNS communicates with the CNS via nerves.
■ The sensory information is acted upon by the muscles and nerves.
● Distinguish among the structures of a neuron.

○ 4 basic structure of the neuron:
1. The soma: Contains the nucleus and many of the organelles.
2. Dendrites: Branched structures attached to the stoma that receives
messages from other neurons.
3. Axon: A long, thin extension of the soma that conveys a message to
the terminal buttons.
4. Terminal buttons: Extensions of the axon that convert the message to a
chemical form by releasing neurotransmitters into the synapse.
● Compare supporting cells in the central and peripheral nervous systems.

○ Support of neurons in the CNS:
■ Astrocytes
■ Oligodendrocytes
■ Microglia
■ They support by creating an environment conductive to neuronal

function, providing a myelin sheath, activating immune responses.
○ Support of neurons in the PNS:

■ Schwann cells provide myelin and facilitate recovery from injury to
neurons.
● Assess the function of the blood-brain barrier

○ The blood-brain barrier protects the CNS, selectively permitting only some
substances to enter.
■ Barrier structure:
● Capillary walls to help regulate the composition of fluids in the
brain, protecting neuronal transmission.
● Capillaries are surrounded by astrocyctes (also help regulate
contents of the fluid surrounding the capillaries).
○ Rich in more permeable in the area postrema, permitting neurons in this region
to detect the presence of a toxic substance.
● Explain the process of neural communication in a reflex.

○ A simple withdrawal reflex is made up of a sensory neuron that detects the
stimulus, a spinal interneuron that excites a motor neuron.
○ Motor neurons cause the withdrawal behavior.
○ This reflex can be modified by input from the brain that can prevent the
withdrawal behavior by inhibiting the motor neuron.
● Describe membrane potential, resting potential, hyperpolarization, depolarization, and

the action potential.
○ Resting potential: -70mV (more negative inside).
○ Hyperpolarization: when the inside of the neuron becomes more negative.
○ Depolarization: when the inside of the cell becomes more positive.
○ Action potential: Occurs when a neuron is depolarized beyond its threshold of
excitation.
■ Threshold is -55mV.
■ It is a burst of depolarization followed by hyperpolarization.
● Summarize how diffusion, electrostatic pressure, and the sodium-potassium pump

help establish membrane potential.
○
● Summarize the series of ion movements during the action potential.
○ After reaching the threshold of excitation, the voltage gated sodium channels
open allowing sodium to enter inside.
○ Sodium ion movement is driven by the forces of diffusion and electrostatic
pressure.
○ The axonal membrane then depolarizes.
○ The positive charge inside the cell opens the voltage gated potassium pumps.
○ Potassium exits the cell due to the forces of diffusion and electrostatic
pressure.
○ As potassium diffuses, the membrane is hyperpolarized → becomes more
negative than the resting potential.
○ → Potassium channels close, stopping the ions from exiting the cell.
○ → Sodium-potassium pumps become active, and establishing resting potential.
● Describe conduction of the action potential.
● Identify the presynaptic structures involved in synaptic communication.

○ Presynaptic membrane faces the postsynaptic membrane across the synaptic
cleft.
○ Presynaptic cells contain synaptic vesicles with neurotransmitters.
■ Transport vesicles fill vesicles with neurotransmitters.
■ Trafficking proteins are involved in releasing neurotransmitters and
recycling vesicles.
● Describe the process of neurotransmitter release.

○ Following an action potential, neurotransmitter is released from vesicles in the
presynaptic cell.
● Contrast ionotropic and metabotropic receptors.

○ Ionotropic receptors: Open ion channels in direct response to the binding of a
ligand.
○ Metabotropic receptors: Indirectly open ion channels through the use of G
protein.
■ They also activate a second messenger system that communicates with
with the nucleus that affects the function of the cell.
■ Second messengers can turn specific genes on or off to initiate or
terminate production of proteins.
● Compare EPSPs and IPSPs in postsynaptic cells.

○ EPSPs: A depolarization resulting from the entry of sodium or calcium ions
into the cell through a neurotransmitter-dependent ion channel.
○ IPSPs: A hyperpolarization resulting from the exit of potassium ions or entry
of chloride ions into the cell through a neurotransmitter-dependent ion
channel.
● Summarize neural integration of EPSPs and IPSPs.

○ If the integrated messages result in depolarization beyond the threshold of
excitation for the cell → the neuron will fire an action potential.
○ If the messages are IPSPs or do not reach the threshold of excitation → the
neuron will not fire an action potential.
● Explain how postsynaptic potentials are terminated.

○ Postsynaptic potentials are terminated by removing a neurotransmitter from
the synapse through reuptake transporters.
■ It can also be terminated through enzymatic deactivation.
● Distinguish autoreceptors from postsynaptic receptors.

○ Autoreceptors: Metabotropic receptors located on the presynaptic membrane
that help regulate the amount of neurotransmitter that is released.
○ Postsynaptic receptors: Located on the postsynaptic membrane and serve to
convey a message to the postsynaptic cell.
● Identify synapses other than those involved in neural integration.

○
● Describe examples of nonsynaptic communication.
○ Neuromodulators: Chemicals released by neurons that travel farther and are
dispersed more widely that are neurotransmitters.
○ Hormones are secreted by cells in endocrine glands or by cells located in
various organs.
Chapter 2: Lecture notes

● Ionic bond (electstatic force)
● Covalent bond (sharing of electrons to form molecules)
○ Carbon chains (e.g. glucose, amino acids, etc.)
■ Peptides: short proteins.
■ Proteins: a sequence of amino acids
○ Phospholipids
■ Negative charge of the “head” makes it hydrophilic.
■ The tail is “hydrophobic”
■ Neuron’s skin is composed of phospholipid bilayers.
● Nerve/neuron cells: global function neurons

○ Neurons’ structure in the soma:
■ Cell nucleus with pores for mRNA transport.
■ ER for production, storage and transport proteins.
■ Golgi apparatus: Post office for packing.
■ Mitochondria: Power plant (generates ATP)
■ Lysosomes: waste processing
■ Microtubli: Road system for transportation neurotransmitter through
axon.
○ The nucleus contains chromosomes with genes in the DNA.
■ Transcription occurs here (genes are read from the DNA and convert it
to mRNA).
■ mRNA then leave the nuclear through the pores.
○ Axoplasmic transport process:

■ Kinesin: Anterograde transport from the cell body (soma) to terminal
buttons.
■ Dyein: Retrograde transport from terminal buttons to soma.
● Glial cells (support cells/glue cells)

○ Microglia: Immunologic defense & removal of dead cells.
○ Macroglia: 3 types
■ Oligodendrocytes: Make myelin sheath in CNS.
● The soma wraps around the dendrites to make myelin sheaths.
● Make more than one myelin sheath.
● Oligodendrocytes provide physical support to neurons and…
● add myelin to neuron axons.
■ Schwann cells: Make myelin sheath in PNS.

● Can only make one myelin sheath on the axon of the neuron.
● physical support is not priority.
■ Astrocytes: Structure and solidity (glue = glia). They isolate synaptic

clefts and feed neurons with glucose.
● Astrocytes have 5 main functions:
○ Providing physical support to neurons
○ Providing isolation of neural contacts. The astrocytes
cover the synapses (points of contact between neurons)
such that signals cannot spill over to other cells in the
direct neighbourhood.
○ Breaking down and engulfing of dead or dying cells
(phagocytosis)
○ Breaking down of some types of neurotransmitters.
○ Providing neurons with energy from the blood stream.
● Bioelectricity: Membrane potential

○ The neuron is more negatively charged on the inside, compared to the outside.
○ Ions move through diffusion and electrostatic force.
■ Diffusion: particles will move from regions with high to low
concentration.
■ Electrostatics: Same charged particles repel each other, oppositely
charged particles attract each other.
○ The membrane contains ion specific channels that are voltage gated (K+, Na+,
Cl-, etc.)
■ Na+ and Cl- want to move in due to diffusion but…
● Na+ go inward by diffusion and electrostatic force.
● Cl- is kept outside because of electrostatic force.
● A- cannot pass through the membrane.
● K+ is kept inside because of electrostatic force
○ Resting potential – no firing neuron

■ Membrane potential is -70mV (to -65mV).
■ Negative charge inside (K+ and A- inside), Positive outside (Na+ and
Cl- outside)
■ K+ and A- want to go out due to diffusion but A- cannot pass the
membrane because there is no gate for these ions and K+ is retained by
electrostatic force.
■ Sodium-potassium pump maintains membrane potential.
■ 2 Na+ bind to the pump and is pumped out, changing the membrane
pump shape allowing K+ ions to bind.
○ Ation potential – firing neuron

■ all-or-none law
■ From resting potential, when the threshold is reached, an action
potential happens.
■ Hyperpolarization: becoming more negative.
■ Depolarization: becoming more positive.
● Action potential mechanism:

○ If the threshold is reached (-55mv), Na+ voltage gated channels open allowing
Na+ ions inside → inside is then less negative (depolarization).
○ K+ channels open allowing K+ inside to go outside of the cell.
○ Na+ channels close (refractory period), Na+ inflow is stopped.
○ K+ channels keep flowing out, cell inside returns to negative (repolarisation)
○ K+ channels close, Na+ channels return to their normal closed condition.
○ → The membrane then temporarily has an extra negative charge
(hyperpolarization).
● Action potential conduction

○ The first action triggers a domino effect.
○ Relatively slow:
○ Energy consuming:
■ An action potential can also be conducted passively → faster but the
signal decay strongly with distance. → saltatory conduction (jumping
conduction).
● The axon is covered with pieces of myelin that prevent
generation of action potentials.
● A new action potential is generated at the myelin interruptions
(nodes of Ranvier).
■ Advantages of saltatory conduction:
● Faster because of the pieces of myelin.
● Energy efficient because there are no action potentials in
myelin regions (only in nodes of Ranvier).
Chapter 3: Structure of the Nervous System
● Apply anatomical terms to the nervous system

○ Neuraxis: Directions in the nervous system are usually described with relative to this;
an imaginary line drawn through the length of the CNS, from the spinal cord up to the
front of the brain.
■ E.g. alligator (straight neuraxis).
■ Anterior: Front end
■ Posterior: Back end (e.g. tail of the

alligator)
○ Rostral: toward the nose and mouth
○ Caudal: toward the tail
○ And Dorsal surface: The top of the head and the
back
○ Ventral surface: faces the ground (belly of the
alligator)
○ Lateral: frontal views (both alligator and humans)
○ Medial: Side views (both)
○ Ipsilateral: Structures on the same side of the body.
○ Contralateral: Structures on opposite sides of the body.
● Compare the locations and functions of the meninges and ventricular system
○ The whole nervous system is covered by tough connective tissue.
○ Meninges: The protective sheaths around the brain and spinal cord (CNS). It consists
of 3 layers:
■ Dura mater: outer layer; thick & tough, flexible but unstretchable.
■ Arachnoid membrane: middle layer; soft & spongy.
■ Pia mater: Lower layer; closely attached to the brain and spinal cord;
contains smaller surface blood vessels of the brain and spinal cord.
● Subarachnoid space: Space between the pia mater and arachnoid
membrane. Gap filled with cerebrospinal fluid (CSF).
○ The PNS is covered with 2 layers of meninges.

■ The arachnoid membrane (with CSF) covers only the brain and spinal cord
(CNS).
■ The dura mater and pia mater fuse and form a sheath that covers the spinal
nerves, cranial nerves, and the peripheral ganglia (PNS).
○ The ventricular system of the brain:

■ A series of hollow, interconnected chambers called ventricles, filled with
CSF.
■ Lateral ventricles are connected to the third ventricle.
● The third ventricle is located at the midline of the brain.
● The third ventricle’s walls divide the surrounding parts of the brain
into symmetrical halves.
■ The cerebral aqueduct connects the third ventricle to the fourth ventricle.
■ These ventricles are important for the production and containment of CSF.
■ Cerebral spinal fluid: Made by special tissue with a rich blood supply called
choroid plexus (which extends to the ventricles).
1. CSF is made by choroid plexus in the lateral ventricles.
2. CSF flows into the third ventricle, where more CSF is produced.
3. CSF then flows through the cerebral aqueduct to the fourth ventricle,
where more CSF is produced.
4. CSF leaves the fourth ventricle through small openings that connect
with the subarachnoid space.
5. CSF then flows through the subarachnoid space around the CNS,
where it is reabsorbed into the blood supply through the arachnoid
granulations.
● Identify the locations and functions of the structures of the telencephalon.

○ The forebrain contains 2 subdivisions:
1. Telencephalon
2. Diencephalon
○ Telencephalon: Includes most of the two symmetrical cerebral hemispheres.

■ Cerebral hemispheres are made up of the cerebral cortex, the limbic system,
and the basal ganglia.
■ The limbic system and basal ganglia are primarily in the subcortical regions
of the brain, located beneath the cerebral cortex.
■ These hemispheres make up the cerebrum.
■ Cerebral cortex: Surrounds the cerebral hemispheres like the bark of a tree.
● Folded; convoluted with sulci (small grooves), fissures (large
grooves), and gyri (bulges between adjacent sulci or fissures) which
help enlarge the SA of the cortex.
● Consists mostly of glia cells, dendrites, and interconnecting axons.
■ Lobes of the cerebral cortex: Regions of the cerebral cortex/

● Frontal lobe (front) - includes everything in front of the central
sulcus.
● Parietal lobe (wall) - located on the side of the cerebral hemisphere,
just behind the central sulcus, lower of the frontal lobe; spatial
information.
● Temporal lobe (temple) - forward from the base of the brain, ventral
to the frontal and parietal lobes.
● Occipital lobe (back) - back of the brain, caudal to the parietal and
temporal lobe.
● Between these sensory regions, we have association cortices, which
this sensory information is further processed.
● Central sulcus: border between the frontal and parietal lobes.
■ Sensory cortex: 3 Areas in the cerebral cortex that receive information from
sensory organs:
● Primary visual cortex - Receives visual information; located in the
occipital lobe, on the inner surfaces of the cerebral hemispheres.
● Primary auditory cortex - Receives auditory information; located in
the temporal lobes, on the lower surface of the later fissure.
● Primary somatosensory cortex - Receives information from the

body's senses.
■ Sensory Association Cortex: The area wherein processes like perceiving,

learning and remembering, planning, and action take place (sensation and
action).
■ (Primary) motor cortex:

● Neurons in this area are connected to muscles in different parts of the
body. They are contralateral (The left primary motor cortex controls
the right side of the body and vice versa).
■ Motor association cortex:
● Located in front of the primary motor cortex.
● This region controls the primary motor cortex, and directly controls
behavior.
■ Prefrontal cortex: Rest of the frontal lobe, involved in formulating plans and
strategies.
○ Diencephalon: In between the telencephalon and the mesencephalon, surrounding the

third ventricle. 2 most important structures:
1. Thalamus
2. Hypothalamus
■ Thalamus: Receives information from the sensory organs OR the neurons

relay the sensory information to specific projection areas of the cerebral
cortex.
■ Hippocampus: Memory
■ Amygdala: Elicits fear, emotional response
■ Basal ganglia: Planned movements.
● Identify the location and functions of the structures of the diencephalon.

○ Thalamus: One of the two most important structures in the diencephalon.
■ It has two lobes, connected by a bridge of gray matter called the massa
intermedia.
■ Neural input is received by the thalamus.
■ It is divided into several nuclei – the neurons in the nuclei either receive or
send sensory information.
○ Hypothalamus: Second most important structure in the diencephalon.

■ Controls the autonomic NS and endocrine system.
■ Organizes behaviors related to the survival of the species (fighting, fleeing,
mating, feeding).
● Identify the locations and functions of the structures of the mesencephalon (midbrain).
○ Midbrain (Mesencephalon): Surrounds the cerebral aqueduct and consists of two
major parts:
1. Tectum
2. Tegmentum
■ Tectum (roof): Located in the dorsal portion of the mesencephalon. Structure

of tectum:
● Superior colliculi
○ Part of the visual system
● Inferior colliculi (appear as 4 bumps on the brain stem)
○ Part of the auditory system
■ Tegmentum (covering): Includes the:
● rostral end of the reticular formation
○ Consists of many nuclei
○ Receives sensory information by means of various pathways.
○ Plays a role in sleep, attention, muscle tone, movements, and
various vital reflexes.
● several nuclei controlling eye movements

● the periaqueductal gray matter
○ Consists mostly of cell bodies of neurons
○ Contains neural circuits that control sequences of movements
that constitute species-typical behaviors.
● the red nucleus and the substantia nigra

○ Axons that arise from the red nucleus constitute one of the
two major fiber systems that bring motor information from
the cerebral cortex and cerebellum to the spinal cord.
○ The substantia nigra contains neurons whose axons project

to the caudate nucleus and putamen
● ventral tegmental area
● Contrast the locations and functions of the structures of the metencephalon and
myelencephalon.
○ Metencephalon: Consists of the cerebellum and the pons
■ Cerebellum:
● 2 hemispheres (like a mini cerebrum)
● Receives visual, auditory, vestibular, and somatosensory information
● Receives information about individual muscle movements being
directed by the brain.
● → Smooths out and coordinates movements.
■ Pons:
● Has a large nucleus that relays information from the cerebral cortex
to the cerebellum.
● Contains a portion of the reticular formation that appears to be
important in sleep and arousal.
○ Myelencephalon: Contains the medulla oblongata
■ Medulla (oblongata): Regulation of the cardiovascular system, respiration,
and skeletal muscle tone.
● Describe the structure and functions of the spinal cord.

○ Spinal cord: A long, tube-like structure that functions to distribute motor fibers to the
effector organs of the body → collects
somatosensory information to be passed on to the
brain.
○ Protected by the vertebral column which is
composed of 24 vertebrae.
● Identify the functions of the cranial nerves.

○ 12 pairs of cranial nerves are attached to the ventral surface of the brain.
■ Vagus nerve: Regulates the functions of the organs in the thoracic and
abdominal cavities. The feeling of the internal organs.
● Differentiate the afferent and efferent axons of the spinal nerves.

○ Afferent axons: The direction of information is inward, towards the CNS.
○ Efferent axons: The direction of information is outward, away from the CNS (PNS)
● Compare the sympathetic and parasympathetic divisions of the autonomic nervous system.
○ Somatic NS: Receives sensory information and controls movements of the skeletal
muscles.
○ Autonomic NS: Regulation of smooth muscle, cardiac muscle, and glands.
■ Sympathetic division
● Fight, flight or freeze
● Using the stored energy
■ Parasympathetic division
● Rest or digest
● Increases the body’ supply of stored energy.
Lecture 3.2: Neuroanatomy

● Development of CNS:
○ Fertilized embryo …
○ Ectoderm: Most outer layer of cells.
■ Folds toward itself, forming the neural
groove and the neural crest.
○ Neural groove: forms the central canal.
■ The central canal forms the spinal cord
and the front part develops into the brain.
● Development of the cortex (ventricular zone/green in the

picture)
○ Radial glial cells in the ‘ventricular zone’ form
extensions outward.
○ Caja-Retzius (CR) cells place themselves against
the pia mater.
○ Neurons climb up along the radial glia until they reach the CR cells (layer).
○ CR cells and pia mater are pushed outward.
● Neural tube to adult brain

○ After 5 years, 95% of the adult brain is formed.
○ Telencephalon (forebrain) - parts and functions

■ Cerebral cortex:
● Surrounds cerebral hemispheres
● Consists mainly of glia and cell
bodies, dendrites, and
interconnecting axons of neurons
● 4 lobes
■ Sensory cortex:
● Primary visual cortex (in the occipital lobe)
● Primary auditory cortex (in the temporal lobe)
● primary somatosensory cortex (in the parietal lobe)
● Insular cortex (information about taste)
■ Sensory association cortex:

● This analyzes information received from primary sensory cortex
■ Motor cortex:
● Primary motor cortex, most directly involved in the control of
movement.
■ Motor association cortex (premotor cortex):
● Directly controls behavior and primary motor cortex.
■ Limbic system
● Hippocampus: memory, learning
● Amygdala: Fear, anger, emotional response.
● Basal ganglia: Collection of nuclei below cortex in the forebrain,
involved in the control of movement, caudate nucleus, putamen,
globus pallidus.
○ Diencephalon (forebrain):
■ Thalamus: receives most neural input except for smell (sensory gateway)
■ Hypothalamus: Controls the autonomic nervous system and endocrine
system. Regulating the body (fight, flight, feed, mate).
○ Mesencephalon (midbrain)
■ Tectum
● Superior colliculi (area in the visual system)
● Inferior colluculi (area in the auditory system)
■ Tegmentum
● Consists of the portion of the mesencephalon beneath tectum.
○ Hindbrain (metencephalon and myelencephalon)

■ metencephalon
● cerebellum: receive visual, auditory, vestibular
● pons: sleep and arousal
■ myelencephalon
● medulla oblongata: contains part of reticular formation; regulation of
cardiovascular system; respiration; skeletal muscle tone.
● CNS anatomy
○ Neuraxis: an imaginary line that runs through the spinal cord.
○ Rostal/anterior: towards the beak/mouth of an animal (upper side of the body)
○ Caudal/posterior: toward the ground/the tail of an animal (lower part of the body).
○ Dorsal: backside
○ Ventral: belly side
● Structure of the nervous system

○ Central Nervous System
■ forebrain = telencephalon = cerebrum
■ thalamus and hypothalamus = diencephalon
■ midbrain = mesencephalon
■ little brain = metencephalon = cerebellum
■ extended marrow = myelencephalon = medulla oblongata
■ Pneumonic: TEL DIE MES MET MY
○ Peripheral Nervous System

■ 12 Cranial nerves
■ 31 pairs of spinal nerves
○ The spinal column (CNS)

■ 3 levels of protection in the spinal cord and brain

1. Pia mater
2. Arachnoid membrane
3. Dura mater
○ The 12 Cranial Nerves (both motor and sensory functions)

○ Diencephalon
■ Thalamus: Rely information for transferring sensory information to the
cortex.
■ Hypothalamus: Autonomic nervous system; survival-fighting, feeding,
mating, fleeing; hormone secretion via pituitary. (below the thalamus).
○ Basal ganglia (set 3 nuclei): motor control, motor learning
■ Stops the motor cortex from doing something if not needed → motor gating.
○ Primary cortices: Specialised in one function (motor, somatosensory, auditory, visual)

○ Association cortices: For combining information; not concerned with sensation and
movement.
○ Relationship between primary and association cortices.
1. Motor association cortex: (plans what to do)
2. Motor cortex: (does it)
3. Sensory cortex (feels the object)
4. Sensory association cortex (combining the information/the parts of the object

to infer what it is).
● Ventricular system
○ Cerebro Spinal Fluid (CSF) circulates through the ventricles and around the brain.
■ Produced by choroid plexus
■ For weight reduction and shock absorber.
○ Hydrocephalus: the narrowing cerebral aqueduct → build-up of cerebrospinal fluid.
Chapter 4: Psychopharmacology and Neurotransmitters

● Differentiate between drug, drug effect, and site of action.
○ Drug: An exogenous (outside the body) chemical not necessary for normal cellular
functioning that significantly alters the functions of certain cells of the body when
taken in relatively low doses.
○ Drug effects: the changes we can observe in an individual’s physiological processes
and behavior.
○ Site of action: The locations where drug molecules bind with molecules located on or
in cells of the body, to affect some biochemical processes of these cells.
● Describe the steps of pharmacokinetics

○ Steps of pharmacokinetics are like describing the life cycle of a drug molecule
in the body.
1. Absorbed: The drug is administered and absorbed through tissues (e.g.

intramuscular injection)
a. Intravenous injection (IV): Injection into the vein → fast and easily
distributed within seconds. Disadvantage – extra skill and care and
because of its rapid effect, if the patient is sensitive to it, there is little
time to inject another drug to counteract it.
b. Intraperitoneal injection (IP): Injected through the abdominal wall
into the peritoneal cavity. – mainly for small lab animals.
c. Intramuscular injection (IM): Injected into a large muscle (e.g. arm,
thigh, buttocks.)
d. Subcutaneous injection (SC): injected beneath the skin.
e. Intracerebroventricular (ICV) administration: Injecting the drug into

a cerebral ventricle to get past the blood-brain barrier. → rapid effects.
f. Oral administration: Drug molecules are absorbed into the blood
through the digestive tract. → then it undergoes first-pass metabolism.
i. = The reduction of the amount of active drug molecules
available to produce an effect.
g. Sublingual administration: Placing a drug beneath the tongue → drug
is absorbed through capillaries.
h. Inhalation: Drugs pass through the lungs to the brain → rapid effects.
i. Topical administration: Drugs enter the body through the skin and its
mucous membranes.
j. Sniffing
2. Distribution within the body: Drug is distributed throughout the body and
blood.
a. Drugs exert their effects only when they reach their sites of action
(most sites in or on the cells of the CNS).
b. The most important factor that determines the rate at which a drug
reaches sites of action is its lipid solubility (to pass through cell
membranes).
3. Metabolized: The drug is changed to an inactive form by enzymes

a. The liver plays an especially active role in the enzymatic deactivation
of drugs, but some can also be found in the blood.
b. Sometimes, enzymes transform molecules of a drug into other forms
that are biologically active → some drugs last very long.
4. Excreted: The drug is excreted in urine by the kidneys.
● Identify why drugs vary in effectiveness and how these differences can be measured.
○ 2 Reasons why drugs vary in effectiveness:
1. Sites of action
a. Different drugs (although they have the same effects) have
different sites of action.
b. E.g.: Oxycodone and aspirin (opioids)

i. Oxycodone suppresses the activity of neurons in the
spinal cord and brain involved in pain perception.
ii. Aspirin reduces the production of a chemical involved
in transmitting information from damaged tissue to
pain-sensitive neurons.
iii. → Oxycodone > aspirin
2. The affinity of a drug with its site of action

a. Affinity: The readiness with which two molecules join together
for the sites to which they attach.
b. High-affinity drug → effects at a low concentration
c. Low-affinity drug → high doses to produce an effect
○ The best way to measure the effectiveness of a drug is to plot a dose-response

curve.
■ IV: doses of the drug, DV: effects of the drug
■ → A larger individual requires a larger quantity of a drug to produce
an effect. This is because drugs distribute themselves throughout the
rest of the body.
■ Increase concentration → increase effect until the max effect is
reached.
○ Therapeutic index: Measure of a drug’s margin of safety.

■ Obtained by administering varying doses of the drug to a group of lab
animals or human volunteers.
● Differentiate between tolerance, sensitization, and withdrawal effects

○ Tolerance: When a drug is administered repeatedly, its effects diminish.
■ Taking the drug more and more for it to be effective because the effects
have diminished.
■ After tolerance, once that individual stops, they will likely experience
withdrawal symptoms.
○ Withdrawal: Experiencing the opposite of the effects after stopping the

administration of the drug (e.g. euphoria drug effect → stops → dysphoria).
■ Physical dependence on the drug once they stop taking the drug
completely.
○ Sensitization: When a drug is administered repeatedly, its effects become

more and more effective.
● Describe a placebo and the placebo effect.

○ Placebo: An inactive substance. They contain no active drug molecule.
○ Placebo effect: The idea that a placebo works and thus affects one’s
physiological state.
■ Informing that a placebo is a stimulant → increases heart rate and
blood pressure.
● Summarize how drugs can affect neurotransmitter synthesis

○ Neurotransmitters (NT) are synthesized by presynaptic neurons.
○ Precursors: Psychoactive drugs that produce their effects by altering the
production of neurotransmitters.
■ Used to increase the amount of neurotransmitter a cell can synthesize
and release into the synapse.
■ → they are agonists because administrating them increases the activity
of the neurotransmitter system.
○ NT synthesis is controlled by enzymes →
■ If a drug deactivates one of these enzymes, it will prevent an NT from
being produced.
■ A drug that deactivates it is then an antagonist.
● Explain the effects of drugs on neurotransmitter storage and release.

○ After production, NT is stored in synaptic vesicles until they are transported to
the presynaptic membrane and released.
○ Vesicle transporters: pump molecules of the neurotransmitter across the

vesicle membrane, filling the membranes. → They move the molecules into
the vesicles.
■ Drugs can block vesicle transporters by binding with a particular site
on the transporter and inactivating it → antagonists.
■ Drugs can bind with these proteins and directly trigger the release of
the neurotransmitter → agonists.
■ → Agonists can directly stimulate the release of a neurotransmitter
from a vesicle.
■ → Antagonists can block vesicle transporters or deactivate the cellular
machinery responsible for vesicle release.
● Summarize the effects of drugs at the receptor.

○ The effects depend on where the receptor is located, what its normal effects
are, and whether the drug activates the receptor or blocks its actions.
○ The most important and complex sites of action of drugs in the NS =>
presynaptic and postsynaptic receptors.
○ Postsynaptic receptors
■ Once a neurotransmitter is released → postsynaptic receptors are
stimulated.
■ Drugs bind with these receptors (either agonists or antagonists).
■ Direct agonists: A drug that mimics the effects of a neurotransmitter.
● They normally attach to the site the NT normally attaches →
same response is triggered.
■ Direct antagonists (receptor blockers): A drug that binds with the
postsynaptic receptors but block them from being activated.
● They occupy the receptor’s binding site (for NT) → NT cannot
bind and activate the receptor.
● These drugs can have therapeutic effects (e.g. for
schizophrenia).
■ Some postsynaptic receptors have multiple binding sites where
multiple molecules can bind to.
● Noncompetitive binding: When a molecule binds to one of the

alternative sites. → prevents the ion channel from opening →
molecules/drug is an indirect antagonist.
● If a drug binds to one of the alternative sites and facilitates the
opening of an ion channel → indirect agonist.
○ Presynaptic receptors
■ Autoreceptors function to modify the activity of the presynaptic cell.
■ Agonist molecules at these receptors result in reduced synaptic
communication.
● Describe the effects of drugs on neurotransmitter reuptake and deactivation.

○ Agonists block neurotransmitter reuptake or deactivation to retain more of the
neurotransmitter in the synapse available to bind to receptors.
○ Drugs can serve as antagonists for teh enzymes that deactivate the NT,
increasing synaptic transmission.
● Neurotransmitters and Neuromodulators

○ 2 amino acids responsible for synaptic communication:
1. Excitatory effects (glutamate)
2. Inhibitory effects (GABA, glycine)
● Compare the features of the amino acid neurotransmitter system.

○ Different neurotransmitters
○ Glutamate
■ Main excitatory NT in the CNS
■ Synthesized from a precursor (glutamine) by an enzyme (glutaminase).
■ After synthesis → stored in vesicles (packed by glutamate
transporters).
■ It is then released from the presynaptic neuron following an action
potential.
■ 4 Major types of glutamate receptors:
1. NMDA receptor (ionotropic)
a. Alcohol is an antagonist of NMDA receptors.
b. at least 6 different binding sites.
c. When open, the ion channel controlled by thsi receptor
permits both Na+ and Ca2+ to enter the cell.
d. Influx of Ca2+ serves as a second messenger binding
and activating enzymes within the cell.
2. AMPA receptor (ionotropic)

a. Controls the sodium channel so when glutamate
attaches to the binding site → EPSPs produced.
3. Kainate receptor (ionotropic)

4. Metabotropic glutamate receptor (metabotropic)
■ Reuptake and deactivation of glutamate

● Removed from the synapse by excitatory amino acid
transporters + broken down into its building block precursor
(glutamine) by the enzyme glutamine synthase.
● Failure to remove glutamate from the synapse can produce
glutamate excitoxicity and damage neurons.
○ GABA
■ Inhibitory NT with widespread distribution throughout the CNS.
■ Produced from a precursor (glutamic acid) by the action of an enzyme
(glutamic acid decarboxylase or GAD).
■ Without the activity of inhibitory synapses, neural connections would

be unstable because neurons would be firing uncontrollably ( →
seizure).
■ Receptors of GABA
1. GABAA receptor (iontropic)
a. Control chloride channels
b. Contain at least 5 different binding sites
i. Muscimol (direct agonist) binds with primary
binding site
ii. Bicuculline (direct antagonist) binds with
primary binding site
iii. Benzodiazepines (anxiety-dissolving/sleep
medications) bind with the second site
iv. Picrotoxin binds with the second site and
inhibits the activity of the GABAA → indirect
antagonist.
■ Deactivated by the enzyme GABA aminotransferase
■ Transported into the presynaptic cell by GABA transporters.
● Summarize the features of the acetylcholine system.

○ Acetylcholine is synthesized by the enzyme choline acetyltransferase
○ Packed into the vesicles by the vesicle ACh transporter.
○ ACh NT:
■ The primary NT is secreted by axons of the PNS that control muscle
contraction.
■ Most acetylcholine-releasing neurons are found in locations in the
CNS – 3 Pathways:
● In the dorsolateral pons
● Basal forebrain
● Medial septum
○ Choline + Acetyl coenzyme A → enzyme ChAT =
Acetylcholine
○ Binds to nicotinic and muscarinic receptors

■ Nicotinic is stimulated by nicotine and is ionotropic.
■ Muscarine is metabotropic.
○ Deactivated by acetylcholinesterase
○ Precursor is transported into the presynaptic cell by choline transporters.
● Summarize the key features of the monoamine system

○ Monoamines are classical NT (a family of relatively small molecules that
includes the monoamines and ACh):
■ Dopamine
■ Norepinephrine
■ Epinephrine
■ Serotonin
■ Histamine
○ Monoamines are synthesized from amino acid precursors, loaded into vesicles
by vesicle monoamine transporters and released after an action potential.
○ Monoamines bind to a variety of ionotropic and metabotropic receptors.
○ Monoamines are deactivated by enzymes like monoamine oxidase.
○ Reuptake transporters, such as the dopamine transporter, norepinephrine
transporter, and serotonin transporter, remove monoamines from the
synapse.
● Contrast the features of peptide neurotransmitters with classical neurotransmitters

○ Classical NT:
■ Synthesized from relatively small amino acid precursors.
■ Stored in vesicles and can be co-released (with Peptide NT) following
an action potential.
○ Peptide NT:
■ Synthesized from large polypeptides.
■ Stored in vesicles and can be co-released (with Classical NT)
following an action potential.
■ Can function as either NT or neuromodulators to regulate the

sensitivity of receptors to classical co-released neurotransmitters.
● Summarize the features of the lipid neurotransmitter systems.

○ Synthesized on demand and thus not stored in vesicles.
○ Endocannabinoids bind to both CB1 and CB2 receptors.
○ Anandamide is deactivated by the enzyme FAAH within the presynaptic
neuron
Lecture #2 notes
● The synapse: contact point (mostly on the dendrites) between the axon and the
receiving cell.
○ Giving cell is presynaptic cell
○ Receiving cell is postsynaptic cell.
○ There is a synaptic cleft (gap) between the post and presynaptic cell.
○ NT from the microtubule (kynacytes) which are released in the terminal
button.
○ NT will interact with the presynaptic membrane → vesicles will bust open and
NT inside will be released in the synaptic cleft = exocytosis.
○ NT attaches to postsynaptic cell → influences behavior (transmitting the
message).
● Exocytosis:
○ Calcium triggers exocytosis.
○ Depolarisation of the presynaptic membrane leads to the opening of the
voltage-gated calcium channels → calcium influx in the cell (terminal button)
→ breaking the vesicles → NT released.
○ Vesicles are torn by protein docks.
● Effect of neurotransmitter release in post-synaptic neuron

○ NT diffuses to the postsynaptic membrane.
○ The postsynaptic membrane has transmitter dependent ion channels →

Ionotropic receptor. (a channel with a “lock” attached to it which only one
key (NT) can open it).
○ Effects: excitatory or inhibitory
■ EPSP: The ability to open a sodium channel (e.g. acetylcholine) →
excitatory neurotransmitter; depoarisation of the postsynaptic cell
■ IPSP: The ability to open chlorine channels (e.g. GABA) → inhibitory
NT; hyperpolarisation of the postsynaptic cell.
○ Metabotropic receptors: costs more energy
■ NT activates teh receptor on the membrane.
■ Receptor activates G-protein
■ G-protein breaks away and activates enzyme, which produces second
messenger.
■ The second messenger opens ion channel.
■ Ions enter/leave cell (EPSP OR IPSP).
■ Second messenger can also influence other components → gene
expression.
○ Regulation of NT concentration
■ Reuptake transporters: pump NT back to the terminal buttons.
■ Enzymatic degradation: The enzyme Acetylcholinesterase (AChE)
splits ACh into Choline and Acetate
○ Autoreceptors: regulate the production and release of NT by the neuron
■ Metabotropic
■ Activate reuptake transporters in the presynaptic cell.
■ Give off chemicals that block calcium channels → vesicles cannot be
opened.
■ Reducing the amount of NT in the synaptic cell == either promoting
reuptake or blocking the calcium channel.
○ A neuron will only fire if there is more excitatory input than inhibitory.
○ Patella reflex: Monosynaptic reflex → sensory neuron → motor neuron →
behavior.
○ Ligands are chemicals that attach to binding sites.

■ → All NT and drugs are ligands.
● Neuromodulators: wander through the brain and synthesize or desentisize complete

neural networks
○ Activate or deactivate the last parts of the cortex
○ e.g. peptide (short strings of amino acids) – hormones.
● Effects of drugs on the synapse

○ Ways of drug uptake
■ Competitive vs non-competitive binding
● Drug binds to the binding site of the NT → either opens or
blocks the ion channel.
● Drug binds to an allosteric site and either opens or blocks teh
ion channel.
○ Locations of operation
■ Precursor: a base substance from which a NT can be made. → agonist.
● More precursor → more NT.
● e.g. AGO: a precursor that creates dopamine.
■ Drugs can deactivate synthetic enzyme; inhibiting the synthesis of NT
→ antagonist.
● Drug deactivates enzyme → less NT.
● e.g. PCPA inhibits serotonin synthesis.
■ Drug prevents storage of NT in the vesicles
● Drug prevents NT uptake by vesicles → less NT in vesicles.
● e.g. reserpine blocks storage of monoamines.
■ Drugs can stimulate the release of NT → agonist
● Drug opens vesicles → more NT in the cleft.
● e.g. black widow spider opens ACh vesicles (muscle
contraction).
■ Drugs inhibits the release of NT → antagonist
● Drug prevents opening vesicles → less NT in synaptic cleft.
● e.g. botox leading to muscle paralysis – less wrinkles.
■ Drugs stimulate the postsynaptic receptors

● Acts as the NT (direct agonists)
● e.g. nicotine
■ Drugs blocks postsynaptic receptors
● Drug blocks postsynaptic receptos → more post synaptic ion
channels closed.
■ Drugs stimulate autoreceptors (originally inhibitory if autoreceptors
are stimulated)
● The drug stimulates autoreceptors → reduces the
production/secretion of NT.
● e.g. apomorphine reduces dopamine secretion treatment for
addiction locations of operation.
■ Drugs block autoreceptors
● Drugs block autoreceptors → increased production/secretion of
NT
● e.g. Idazoxan blocks norepinephrine autoreceptor, increased
alertness/antidepressant.
■ Drug inactivates acetylcholinesterase → AGO
● Drug blocks enzymes that break down NT → more NT remains
in the cleft.
Chapter 6: Vision
● 25% of our brain capacity is dedicated to the visual system.
○ Basal (stimulus’ color, lines, angles, etc.) → high order (what is it? where is
it?) → associations (inferences/putting everything together).
● Sensation: The detection of physical stimuli and the transmission of this information
to the brain.
○ This involves cells of the NS that are specialized to detect stimuli from the
environment.
● Stimulus: What our eyes can see (no meaning).
● The eye is a sense organ with receptors.
○ Ganglion cells: Neurons whose axons travel through the optic nerves and carry
visual information to the rest of the brain.
○ Amacrine cells: Cells that transmit information in a direction parallel to the
surface of the retina and combine messages from bipolar cells next to each
other.
○ Bipolar cells: Neurons whose two arms connect the shallowest layer (ganglion
cell layer) and the deepest layer (photoreceptor layer).
○ Horizontal cells: Transmits information in a direction parallel to the surface of
the retina and combines messages from photoreceptors next to each other.
○ Cones: Photoreceptors responsible for colors, daytime vision and sharpness.
■ Blue, green and red
○ Rods: Photoreceptors responsible for nighttime vision, black and white only.
■ rod opsin + retinal → more sensitive to greenish light.
○ Receptive fields: An area in which a visual stimulus must be located to
produce a response in that neuron. (if it is within the visual field → a neuron
will fire)
■ It is a region of space where a stimulus induces a change in firing
frequency.
■ Light splits chemicals in receptors and produces a change in membrane
potential
● Transduction: The process by which sensory stimuli are converted to neural

(electrical) signals the brain can interpret.
○ This occurs in photoreceptors because it allows light to be converted
into a change in membrane potential.
○ lamellae: thin plates of a membrane that make up the outer segment of
individual photoreceptors, containing photopigments.
■ When light hits, photopigments are split.
○ photopigments: molecules consisting of an opsin (protein) and a retinal
(lipid from Vit A).
■ Rods have rhodopsin as photopigments.
■ Cones have … as photopigments:
● Cyanolabe (blue)
● Chlorolable (green)
● Erythrolable (red)
● Coding: The light intensity (brightness) – rods

○ When rhodopsin (in rodes) is exposed to light, it breaks down into rod
opsin and retinal → triggering a cascade of intracellular events that
hyperpolarize the photoreceptor membrane.
■ Rods hyperpolarize in response to light and depolarize in
response to darkness.
○ Coding is determined by the number of action potentials per time unit.
■ Low intensity → few action potentials.
■ High intensity → many action potentials.
○ Rebound effect: When visual cells have been stimulated or inhibited

for a longer time, they will fire at a slower/faster rate than normal →
afterimage (opposite colors)
○ ON cells
■ Active when light hits the center of the receptive field →
neuron will fire.
■ Inhibited neuron when light hits surround.
■ Activity increases in illumination.
○ OFF cells
■ Inhibited neuron when light hits the center of the receptive
field.
■ Active neuron (firing) when light hits the surround.
■ Activity increases in darkness.
● Coding: light frequency – cones

○ Trichromatic Coding: According to this, color vision results from
activity in three types of cones that are sensitive to different
wavelengths (SML cones). (One cone for short, one for medium, and
one for long wavelengths).
○ Opponent-Process Theory: According to this, red and green are

opponent colors, as are yellow and blue. Staring at one color causes
receptor fatigue. Looking elsewhere then leads to unfatigued receptors
for the ‘opposing’ color to produce an afterimage.
■ Red-green: Ganglion cells activated by red, and inhibited by
green.
■ Yellow-blue: Ganglion cells activated by yellow, and inhibited
by blue.
○ Protanopia: Confusion of red and green – both look yellow

○ Deuteranopia: Confusion of red and green - ????

○ Tritanopia: Seeing the world in greens and reds
■ → Retina lacks ‘blue’ cones.
○ Monochromatic vision: seeing the world in black, grey, and white
■ → retina completely lacks cones.
● Projection to cortex
○ Orientation detection: Occurs primarily through neurons in the striate
cortex, when the stimulus is positioned in the cell receptive field and is
in a specific position, the cell will fire.
■ When cells fire frequently on a specific orientation, then that
cell is sensitive to that position.
■ Every cell is sensitive to a specific orientation.
● Adjacent cells have adjacent receptive fields.
○ Movement detection:
■ Simple cortical cells combine information from LGN cells.
● Simple cells will fire consecutively in case of
movements.
■ Complex cells combine information from simple cells.
● Detect movement.
○ Location detection:
■ Retinotropic organization: Specific regions of the visual field
project to specific parts of the thalamus and visual cortex.
○ Depth detection:
■ binocular disparity: each eye sees a stimulus in a slightly
different location because of the space in between our eyes;
produces images on slightly different parts of the retina of each
eye.
● Shift in the background gives the perception of depth.
● High order processing

○ Thalamus layers:
■ Parvocellular: Colors red and green, high spatial resolution, low
temporal
■ Koniocellular: Color blue, low spatial and temporal resolution.
■ Magnocellular: No colors, low spatial resolution, high
sensitivity to contrast and temporal resolution.
○ Ventral stream: (what the object is)

■ Color perception
● Damaged area V4 leads to impaired color constancy
(ability to perceive the same color in different light
condition).
● Damaged area V8 leads to impaired color vision, color
imagination, and color memory → cerebral
achromatopsia.
■ Object recognition
● Apperceptive agnosia: Problem with recognizing
objects.
■ Face recognition
● Prosopagnosia: Problem with recognizing faces.
■ Extricate body are.
○ Dorsal stream: (where and how the object is)

■ Spatial awareness
● Lateral and ventral: visual attention and eye movements
■ Movement perception
● VIP and medial (MIP): Visual control of grasping and
pointing.
● Akinetopsia: Inability to perceive movement → lesion
in an area of the medial temporal lobe (MT in V5)
■ Visuomotor coordination
● Anterior (AIP): Grasping and manipulating with hands.
● Caudal (CIP): Depth perception.
Chapter 8: Movement
● Anatomy of muscles
○ Alpha motor neuron: Activate extrafusal muscle fiber.
○ Extrafusal muscle fiber: Provide muscle’s motive force (do the work).
○ Intrafusal muscle fiber: Give info on whether the muscle is relaxed or
contracted.
■ These detect the length of the muscles
■ Sets of intrafusal muscle fibers make up spindle
fibers.
■ Sensory endings are wrapped around them.
○ Gamma motor neuron: Activate intrafusal muscle
fibers.
■ GMN’s are more active during complex actions.
○ Golgi tendon organ: These contain stretch receptors to
provide information about how much force is on the
muscle.
■ Can activate inhibitory interneuron if risk of tearing the muscle.
○ Muscle fibers: They consist of myofibers consisting of actin and myosin.
● Activation of muscle spindles (MS) and Golgi tendon organ (GTO)

○ Muscle Spindles 1: Slow change in muscle length (slow, passive)
○ Muscle Spindles 2: Fast change in muscle length (abrupt, rapid)
○ GTO: Change in muscle tension (weight puts pressure/tension on muscle)
● Muscle contraction
○ The terminal buttons of the neurons are connected to motor endplates in the
neuromuscular junction.
○ An action potential arrives at the neuromuscular junction and releases
acetylcholine.
■ The release of acetylcholine causes depolarization of the postsynaptic

membrane.
■ Depolarized postsynaptic membrane → endplate potential.
■ Endplate potential: Induces contraction of twitch of muscle fibers.
○ Voltage-gated Ca2+ channels open → calcium influx in the cytoplasm.
○ The influx of calcium permits myofibrils to extract energy from ATP.
■ And it opens up binding sites on the actin.
○ Myosin heads bind the binding sites of the actin creating cross bridges.
○ These cross bridges are stimulated to move (bend in one direction, detach,
bend back and reattach to another binding site).
○ The strength of muscle contraction is determined by the firing rate of various
motor units.
■ Alpha motor neurons are connected to etxrafusal muscle fibers.
○ Agonist (muscle): Muscles that make the movement.

○ Antagonist (muscle): Muscles that stop the movement (they prevent
overshooting).
● Monosynaptic stretch reflex

○ Help maintain posture and body position.
○ Afferent (to the brain) impulses are conducted to terminal buttons in the gray
matter of the spinal cord.
○ Terminal buttons synapse (connect) to alpha motor neurons.
○ The alpha neuron sends the signal to extrafusal muscle fibers.
● Polysynaptic inhibitory reflex

○ If there’s too much force on a muscle
○ Inhibitory interneurons release glycine and produce inhibitory postsynaptic
potentials on alpha motor neurons.
○ …
● Control from the motor cortex

○ Primary motor cortex: Somatotopic organization; particular parts are
responsible for the movement of specific body parts (more lateral areas control
higher parts of the body).
○ Supplementary motor (SNA): Involved in learning and performing behaviors

consisting of sequential movements (playing an instrument).
○ Premotor cortex: Involved in learning and planning responses that are signaled
by the presence of arbitrary stimuli (swatting a fly).
○ Lateral group: For independent limb movements, particularly hands/fingers.
■ Rubrospinal tract (via red nucleus): Older system; responsible for very
basic movements → lower arms, hands, lower legs, feet.
■ Corticobulbar tract: Projects onto medulla, nerves control movements
of the neck, face, parts of eye movements, and tongue.
■ Lateral corticospinal tract: Fibers crossover to the contralateral spinal
cord, responsible for finer movements → arms, hands, fingers, legs,
feet, toes.
○ Ventromedial group: For balance (body posture) and walking, control
automatic movements.
■ Vertical corticospinal tract: Control muscles that move muscles of the
upper legs and trunk.
● Cerebellum
○ Pontine nucleus: Relay station to give information of planned movements for
the motor cortex to cerebellum → computes how long each muscle contraction
should be for smooth movement.
○ Dentate nucleus: The Cerebellum sends information on how long each muscle
contraction should be via the dentate nucleus to the ventrolateral thalamus,
which projects to the primary motor cortex.
■ The cerebellum can modify ongoing movements (it sends information
to red nucleus via dentate nucleus).
■ Helps control independent limb movements.
○ Damage cerebellum → tumors → problems with timing of antagonists and

agonists muscles → not activates at the right time.
● Higher order control: Motor association cortex

○ Supplementary motor area (SNA): For planning movement sequences.
■ E.g. active during ‘push-and-pull’ sequence.
○ Premotor cortex (PMC): For planning individual (complex) movements that
are guided by sensory information.
■ Uses arbitrary information.
○ Damaged parietal lobe:

■ Left damage: own body
● apraxia: inability to imitate or produce movements in response
to verbal instructions
● limb apraxia: movement of wrong part of limb; incorrect
movement of correct body part; correct movements but in
wrong sequence; especially difficult to imitate actions –
improves when given tools to demonstrate.
■ Right damage: representation of the outside world

● constructional apraxia: difficulty drawing/copying pictures or
assembling objects; more visual problems; don’t see
connections between individual parts and whole object.
● Basal ganglia: motor gating

○ The basal ganglia regulate which actions will be executed (in all generations
of motor actions).
○ Globus pallidus: sends output to motor nuclei in the brainstem, primary- and
premotor cortex, and to SNA via the thalamus.
○ Direct pathway: Promotes motor activity

■ Cortex activates caudate nucleus and putamen.
■ Caudate nucleus and putamen inhibits globus pallidus internal.
■ Globus pallidus internal can’t inhibit thalamus → thalamus is excited.
■ Thalamus excited motor cortex.
○ Hyperdirect pathway: Quickly stopping movement

■ Cortex activates subthalamic nucleus
■ Subthalamic nucleus activates globus pallidus internal
■ Globus pallidus internal inhibits thalamus
■ Thalamus inhibits motor cortex
○ Indirect pathway: Inhibits motor activity

■ Cortex activates caudate nucleus and putamen
■ Caudate nucleus and putamen inhibits globus pallidus external
■ Globus pallidus external activates subthalamic nucleus
■ Subthalamic nucleus activates globus pallidus internal
■ Globus pallidus internal inhibits motor cortex.
○ Influence of substantia nigra: Black substance containing a lot of dopamine.

■ 2 Types of dopamine receptors in caudate nucleus and putamen.
● D1: Excites direct path by opening Na+ channels.
● D2: Inhibits indirect path by opening Cl- channels.
■ Makes sure that during activity, the direct pathways stay ‘open’.
● Parkinson’s disease
○ Basal ganglia disorder
○ Rigidity and tremor → agonist and antagonist go back and forth
○ Tremors subsides during purposeful movement.
○ Activating and stopping movement is difficult = loss of dopominergic neurons
in substantia nigra.
● Huntington’s disease
○ Basal ganglia disorder
○ Hereditable, involuntary movements
○ Every intention to move is carried out
○ Impaired function of indirect pathway = neurons missing in caudate nuclei and
putamen.
Chapter 9: Sleep and Biological Rhythms

● Sleep stages
○ EEG during sleep indicates 5 sleep stages.
1. Awake: Alpha (8-12Hz) and beta (13-30 Hz)
waves; rapid oscillations.
2. Stage 1: Theta waves, lower frequency →
amplitudes are larger because multiple neurons
have similar activities. – 10min in.
3. Stage 2: Sleep spindle, rapid activity →
K-complexes – already asleep but often not
conscious of it yet. – 15min in.
4. Stage 3 and 4: Delta activity, slow wave sleep
5. REM (paradoxical sleep): Theta and beta activity
→ similar to being awake, but muscle activity is
inhibited (except for eyes).
a. About 20 min → back to stage 2.
● Stage 3 and 4: Slow wave sleep

○ Strong suppression of external stimuli → strong stimuli to wake you up.
○ Low probability of waking up spontaneously

■ Once awake → drowsy and disoriented
○ 20% chance of dream recall, often nightmares/dreams withs strong emotions.
● REM Sleep characteristics

○ Rapid eye movement
○ EEG desynchronization – lost of fast/high frequency signals
○ Ponto Genicular Occipital (PGO) waves occur just before REM sleep
○ Paralysis of skeletal muscles
○ Increased genital activity (not erotic)
○ Strong suppression of external stimuli (except for meaningful sounds).
○ High probability of waking up spontaneously → alert.
○ Narrative dreaming → illogical because frontal lobe activity is absent which is
responsible for making sense of situations. 75-95% chance of dream recall.
● Sleep disorders
○ REM sleep behavior disorder
■ Inhibition of motor system (atonia) during REM is impaired
■ Dreams are acted out.
○ Narcolepsy – problems with flip flop system

■ Sleep attacks – cataplexy (antonia-muscle inhibition during wake →
muscle paralysis) → particularly triggered by emotions.
■ Hypnagogic hallucinations: When you are lying in your bed awake,
and start hallucinating (or dreaming) and muscle paralysis.
■ Cause: abnormality in orexin, gene knock-out/poison, neuropeptide
orexin missing.
○ Slow-wave sleep disorders

■ Sleepwalking (somnambulism)
■ Bed-wetting (nocturnal enuresis)
■ Nightmares (pavor nocturnes)
● Function of sleep
○ Each mammal + birds need sleep (for dolphins, each brain hemisphere takes
turn in sleeping)
○ Sleep deprivation
■ Lack of sleep
● leads to: loss of thermoregulation (can’t keep body temperature
up), increased fat and sugar metabolism which causes severe
weight loss, immune system disruption.
■ ‘Voluntary’ deprivation (less than 10 days)
● No physical problem but can lead to cognitive problems (e.g.
concentration)
● Sleep is required for recovery of the brain.
○ Physical recovery does not seem to be the main function of sleep because even
sleep deprived, we can still perform physical activities.
○ Slow-wave: primarily restorative

■ Build up of sugar supply of glycogen in astrocytes – to fuel brain cells
■ Astrocytes give off adenosine to slow brain activity → broken down
during sleep.
■ Learning (consolidation of declarative memory) = specific events you
can consciously talk about.
○ REM: brain development and survival

■ Alertness - animals can stay cautious and somewhat aware.
■ Brain development, reduction in proportion of REM sleep with age.
■ Learning (consolidation of non-declarative memory) = primarily of
actions or procedural things.
● Physiological mechanisms of sleep

○ Adenosine is released when neurons use glycogen.
■ Adenosine: Neuromodulator that inhibits cells when energy is low
■ Adenosine accumulates through the day and is broken down during
sleep.
○ Control of arousal/alertness
■ Acetylcholine:
● Location of neurons that have these NT’s: pons, basal
forebrain, septum-hippocampus.
● Firing rates: Wakefulness – high rate, slow-wave sleep, REM –
high rate
■ Norepinephrine:
● Location: Locus coeruleus (LC) in dorsal pons
● Firing rates: wakefulness – high, slow-wave sleep, REM –
almost zero.
■ Serotonin:
● Location: Raphe nuclei in medulla and pons
● Firing rates: Wakefulness – high, slow-wave sleep, REM – low
■ Histamine:
● Location: Tuberomammilary nucleus in hypothalamus.
■ Orexin:
● Location: lateral hypothalamus
● Activates the brain by activating the other 4 neuromodulators.
○ Control of slow-wave sleep

■ To promote sleep, arousal systems are inhibited (GABA) by neurons in
an area of the anterior hypothalamus
● Ventrolateral preoptic area (vlPOA - a sleep promoting region)
■ vlPOA inhibited by arousal system: flip-flop
■ Orexin neurons stabilize the flip/flop → activates arousal systems that
keep you awake.
■ vlPOA have adenosine receptors = the accumulation of adenosine
during the day promotes sleep → caffeine blocks receptors = no sleep.
■ Waking is stimulated by biological clock, and hunger →

● Activation of orexin neurons.
■ Sleep in stimulated by satiety signals (being full)
● Inhibition of orexin neurons.
○ Control of REM sleep

■ REM-ON: Sublateral nucleus (SLD) + ventral locuscoeruleus
● Emotions via the amygdala can turn on REM-ON.
■ REM-OFF: Ventrolateral periaqueductal gray matter (vlPAG)
○ Interaction between slow-wave and REM flip-flops

■ Sleep begins after activation of vlPOA.
■ vlPOA inhibits orexinergic neurons and REM-OFF region.
■ REM-ON becomes active and starts REM
■ REM-ON region can also be activated by emotional stimuli via
amygdala (brain interprets emotions as start of a dream)
● Sleep-wake rhythm
○ Follows a 24h rhythm (circadian = circa one day)
○ Light, sound, temperature, social interactions, diet patterns, synchronize clock
to 24h
○ Biological clock = 25h
■ Localized in suprachiasmatic nucleus (SCN) of the hypothalamus,
active-awake. Taking SCN away leads to:
■ lesions in SCN which leads to loss of sleep-wake cycle.
■ Transplant of SCN tissue recovers sleep-wake cycle
■ Each SCN cell has its rhythm and they synchronize through
communication.
■ Clock mechanism: Modulation concentration of proteins in the SCN
cells that influence the firing rate of the cells.
○ Seasonal rhythm
■ The pineal gland produces melatonin during the night
● Light inhibits melatonin production

■ Longer nights → less light → less inhibition of pineal gland → more
melatonin → more sleep
Chapter 11: Emotions

● Darwinistic view
○ Emotions: The response of our brain to a positive or negative event, which results in
a certain behavior and physiological response.
○ Consequences of emotional response on survival are important in natural selection.
● 6 Basic emotions
○ Neutral, anger, disgust, fear, happiness, sadness, surprise
○ Emotions are inborn (not learned).
○ Negative emotions (i.e. fear, anger, disgust, etc.) have been studied the most because
it is important for disorders like anxiety and depression.
○ Amygdala is related to the generation of responses.
■ physiological response: faster breathing, hormone released
■ behavioral response: Facial expression, arousal
● Fear conditioning
○ Light associated with shock → light goes on → stress response
● Amygdala
○ Facilitaties behavioral and physiological response
■ Patients with damage on their amygdala does not sweat in anticipation.
○ Difference in emotional vs neutral information processing.
■ Amygdala is more active with fear stimulating words.
● Stress responses
○ Lateral hypothalamus
■ Activation of the sympathetic nervous system → increased heart rate
○ Dorsal motor nucleus
■ Parasympathetic inhibition→ urination, heart beat slows
○ Paraventricular nucleus
■ Hypothalamic pituitary adrenocortical axis (HPA-axis) → stress hormones

released, glucocorticoid secretion.
● Hypothalamic pituitary adrenocortical axis (HPA-axis)

1. Stress signal from amygdala/hippocampus activates paraventricular hypothalamic
nucleus.
2. Hypothalamus produces corticotropin releasing hormone (CRH)
3. CRH stimulates pituitary to secrete adrenocorticotropic hormone (ACTH) in the
blood.
4. ACTH stimulates the adrenal gland to produce cortisol.
5. Cortisol breaks down proteins in the muscle to release glucose for physiological
awareness – immune system weaker → more prone to illnesses.
6. Cortisol also inhibitis the hypothalamus and pituitary (suppreses additional cortisol
production).
● Ventromedial prefrontal cortex (function)

○ Important for controlling emotional behavior
○ Can modulate the expression of fear in different circumstances.
○ Involved in extinction of conditioned emotional response.
○ Plays a role in social/moral decisions.
○ Patients with vmPFC lesions often make a rational choice (lack of emotion).
● Hippocampus (functions)
○ We can learn that specific stimulus/events have negative consequences even without
having encountered it.
○ Focusing too much on possible consequences leads to stress.
○ Chronis stress/depression
■ Leads to overactivation of HPA-axis and increased cortisol levels
○ Too much stress → more cortisol → activity of the HPA-axis is suppressed.
○ Long term stress (inhibits amygdala and hippocampus) can lead to volume loss in
hippocampus or amygdala.
○ Cortisol inhibits the hippocampus by reducing influence of negative memories on
emotional response.
● Effects on immune system

○ Immune system uses lymphocytes which communicate using cytokines.
○ Cortisol interferes with cytokines signals and suppresses immunesystem.
○ People with more Psychological stress are more susceptible to colds.
● Emotions as subjective concepts

○ James-Lange Theory
■ Events in the environment lead to psychological responses such as increased
muscle take, dry mouth, sweating, or increased heart rate.
■ Emotional feelings are a consequence of teh awareness of these physiological
responses.
■ Physiological responses are due to the emotional feelings
■ STIMULUS → PHYSIOLOGICAL RESPONSE → EMOTION
○ 2 types of face emotions:

1. Spontaneous (automatically)
a. Initiated in both hemispheres by subcortical regions.
b. Emotional paresis: There is a lesion in the white matter →
spontaneous is lopsided.
2. Voluntarily (on command)
a. Initiated in left motor cortex
b. Volitional paresis
○ Physiological responses are emotional facial expressions are strongly coupled.
■ → After facial expression → physiological body response will follow.
○ Mirror neuron system → empathy (we tend to imitate others’ emotions).
Chapter 13: Learning and Memory

● Basic types of learning
○ Perceptual learning: Better and faster identification of face/objects if it has been seen
before.
■ Strengthening of network connections.
○ Stimulus-Response learning
■ Classical conditioning: Coupling stimulus to a reflex.
○ Instrumental conditioning: There is purposeful behavior to obtain a reward or a
punishment.
■ Reward vs punishment
○ Motor learning: procedural learning which muscles to activate to obtain a goal.
○ Relational learning: Explicit memory
■ Relations in time, concept and space.
● Perceptual, motor and S-R learning
● Pavlov’s classical conditioning

○ Learning a relation between 2 stimuli: neutral stimulus becomes important
when coupled with meaningful stimulus.
○ Stimulus-Response: Conditioned stimulus induces automatic response.
● S - R learning at neural level (e.g. Pavlov’s experiment)

○ Food induces salivation (herdwired connection between neurons that detect
food and neurons that induce salivation).
○ Sound bell: no response → weak connection between the neurons that detect
the bell sound and those that induce salivation.
○ Repetition → sound bell induces salivation because the synapses connecting
the sounds and neurons that induce salivation have ben strengthened.
● (Donald) Hebb Rule

○ If a synapse (of the pre and post-synaptic neurons) is active at about the same
time that the post-synaptic neuron is active, the synapse will be strengthened.
● Long Term Potentiation: Synaptic strengthening

○ Studied in hippocampus → memory was damaged but epilepsy was cured.
○ NMDA receptors: involved in making connection stronger in LTP; important
for learning.
○ Requirements for LTP:
1. Axon active (secretion of glutamate in synaptic cleft)
2. Depolarisation postsynaptic neuron.

○ NMDA receptors open → Ca2+ enters the receiving cell and
1. Works as 2nd messenger
2. Activated the enzyme CaM-KII to add new AMPA receptors.
a. AMPA receptors delivered to membrane in vesicles.
● Does LTP optimisation make you smarter?

○ Experiment on transgenic mice with enhanced NMDA receptors
■ Platform searching.
● 2 Types of reinforcement
○ Positive reinforcement: Adding a stimulus to promote behavior.
○ Negative reinforcement: Taking away something to promote behavior.
● 2 Types of punishment
○ Positive punishment: Addition of a stimulus leads to decreased frequency of behavior.
○ Negative punishment: Removal of a stimulus leads to decreased frequency of
behavior.
● Experiments
○ Skinner trained the pigeons to play pingpong by operant conditioning (Skinner)
○ Olds and Milner’s study of electrical stimulation of the brainstem reticular formation
could improve spatial navigation in rats. → Rats liked the place that led to stimulation
of electric.
● Serial memory model

○ Event induces neural activity pattern → change in
synaptic connections = memory.
○ Senses → sensory memory → working memory →
long-term memory (encoding).
● Long term memory

○ Non-declarative memory you are not aware of.
■ Procedural memory
■ Conditioning
■ Perceptual
■ etc.
○ Declarative memory: you are aware of and can be verbally exposed.
■ Episodic
■ Semantic memory
○ Patients with hippocampal damage implicit learning is intact
● Reconsolidation of memories
○ During reconsolidation, the old memory is retrieved and adjusted → memory is
vulnerable in this stage.
● Anterograde amnesia is the loss of relational learning ability.
Chapter: Language
● Lateralization
○ Contribution of left to right hemisphere in language learning
○ In most people (90%), left hemisphere is dominant for language but this does not
mean the right hemisphere is not working.
○ WADA test: a test for hemispheric dominance by selectively anesthetising one
hemisphere with sodium amytal → it is invasive.
■ Anesthetizing a hemisphere and controlling is language still works if one is
disabled.
■ Alternatives: TMS or neuroimaging (fMRI) which are less invasive.
○ Right hemisphere dominance for recognizing emotion through neuroimaging.
■ Listening to normal speech vs only prosody (meaningful components filtered
out → just onomatopoeia).
■ Results: listening to prosody – right hemisphere, listening to normal speech –
left hemisphere.
● Organization language processing

○ Wernicke-Geschwind model: Highly influential in the world dedicated to
understanding language function.
○ Speech
1. Speech processed in the primary auditory cortex
2. Wernicke’s area (area behind the primary auditory cortex) becomes active to
recognize the sound.
3. Posterior brain areas will then find the word meaning.
4. Connection between Wernicke and Broca allows for the transmission of the
word sounds.
a. Extra connection for the transmission of word meaning which is
another route.
5. Everything ends up in Broca’s area which is a region of premotor cortex for
planning speech, in right word order: grammar.
6. The plan made can then be conveyed to the motor control to produce speech.
○ Writing
■ Reading the words activate the primary visual cortex → visual info is
converted to sound code.
■ Wernicke’s area becomes active to recognize the sound.
■ Posteriori brain areas will then find the word meaning.
■ Connection between Wernicke and Broca to transmit the word sounds + word
meaning.
■ → Broca’s area which is a region of the premotor cortex plans the speech.
■ Plan can then be conveyed to the motor control to produce speech.
○ Language is unique to humans → we can only study our language.
● Language disorders (aphasia)

○ Tumors
○ Epilepsy
○ Bleeding/infarct (Cerebro Vascular Accidents)
○ Developmental disorders
○ Neurodegeneration (alzheimers, parkinson, etc.)
○ Infections
○ Pure word deafness (PWD)

■ Problems with Wernicke’s area
○ Problems with posterior area regions
■ Transcortical sensory aphasia (TSA) – problems with finding the meaning.
○ Wernicke’s aphasia
■ PWD + TSA leads to this disorder
■ No understanding of spoken or written language.
○ Anomic aphasia
■ Memory whole words
○ Conduction aphasia
■ Damage on the connection between Wernicke and Broca (Arcuate fasciculus)
→ inability to say the word back.
○ Broca’s aphasia
■ Damage on the Broca → planning speech and grammar/motor plans
damaged.
■ Disarticulation
■ Poorly constructed sentences
○ Transcortical sensory aphasia
■ No understanding of spoken or written language. No connection between
word and word meaning.
○ Anomic aphasia
■ Fluent speech and good understanding, but during speech some words cannot
be found in memory.
■ Damage in inferior temporal lobe.
● Reading (vs. hearing)

○ Hear words
■ auditory left hemisphere is activated.
■ Auditory association cortex activated to couple symbols with sounds.
■ Wernicke activated
■ Broca activated
○ Visual words
■ primary visual cortex is activated.
■ Visual association cortex is activated to couple symbols with sounds.
■ Wernicke activated
■ Broca activated
○ 2 Pathways for reading
○ Reading problems: Surface dyslexia

■ Recognizing words in one as a whole is not possible anymore.
■ Patients need to sound out other letter by letter.
■ Problems with whole-word recognition pathway
■ Ventral stream
○ Reading problems: Phonological dyslexia

■ Patients can only read words they already know.
■ Problems with the letter recognition pathway.
■ Dorsal stream
○ Reading problems: Direct dyslexia

■ Analogue of transcortical sensory aphasia for hearing words. Damage on the
posterior brain regions.
■ Patient cannot communicate verbally (meaningless speech + inability to
understand other people’s speech).
● Writing
○ Orthographic dysgraphia
■ No access to whole-word image → not knowing how words look on paper.
■ Spenning is based on sounds → many errors.
○ Phonological dysgraphia
■ Cannot spell based on sounds
■ Problems with writing new words.

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Biological and Cognitive Psychology: Book Notes

Lecturer: Dr. Dennis van ‘t Ent and Dr. Richard Godijn

Tutor: Linda Bettelli

Literature: Physiology of behavior (13th edition)

Biological and Cognitive Psychology: Summary

● Summarize historical and contemporary contributions to behavioral neuroscience

■ In answering these questions, people followed 2 different approaches:

■ Contribution of Rene Descartes on the mind-body question

■ 1870: Physiologists Gustac and Hitzig applied weak electrical current

○ Contributions from anatomy: Structure of the nervous system

○ Contemporary research contributions

● Describe the role of natural selection in the evolution of behavioral traits.

● Identify factors involved in the evolution of human brains.

● Outline reasons for the use of animals in behavioral neuroscience research.

● Identify mechanisms for oversight of animal research.

● Discuss ethical considerations in research with human participants.

● Identify mechanisms for oversight of human research.

● Identify careers in behavioral neuroscience.

○ Individuals pursuing careers in neuroscience work in academia or industry and

● Describe effective learning strategies for studying behavioral neuroscience.

Chapter 2: Structure and Functions of Cells of the Nervous System

● Distinguish among the structures of a neuron.

● Compare supporting cells in the central and peripheral nervous systems.

■ They support by creating an environment conductive to neuronal

○ Support of neurons in the PNS:

● Assess the function of the blood-brain barrier

● Explain the process of neural communication in a reflex.

● Describe membrane potential, resting potential, hyperpolarization, depolarization, and

■ It is a burst of depolarization followed by hyperpolarization.

● Summarize how diffusion, electrostatic pressure, and the sodium-potassium pump

● Describe conduction of the action potential.

● Identify the presynaptic structures involved in synaptic communication.

● Describe the process of neurotransmitter release.

● Contrast ionotropic and metabotropic receptors.

● Compare EPSPs and IPSPs in postsynaptic cells.

● Summarize neural integration of EPSPs and IPSPs.

● Explain how postsynaptic potentials are terminated.

● Distinguish autoreceptors from postsynaptic receptors.

● Identify synapses other than those involved in neural integration.

Chapter 2: Lecture notes

● Nerve/neuron cells: global function neurons

○ Axoplasmic transport process:

● Glial cells (support cells/glue cells)

■ Schwann cells: Make myelin sheath in PNS.

■ Astrocytes: Structure and solidity (glue = glia). They isolate synaptic

● Bioelectricity: Membrane potential

○ Resting potential – no firing neuron

○ Ation potential – firing neuron

● Action potential mechanism:

● Action potential conduction

Chapter 3: Structure of the Nervous System

● Apply anatomical terms to the nervous system

■ Posterior: Back end (e.g. tail of the

○ The PNS is covered with 2 layers of meninges.

○ The ventricular system of the brain:

● Identify the locations and functions of the structures of the telencephalon.

○ Telencephalon: Includes most of the two symmetrical cerebral hemispheres.

■ Lobes of the cerebral cortex: Regions of the cerebral cortex/

● Primary somatosensory cortex - Receives information from the

■ Sensory Association Cortex: The area wherein processes like perceiving,

■ (Primary) motor cortex:

○ Diencephalon: In between the telencephalon and the mesencephalon, surrounding the