Lecture 1 - Introduction
Theoretical View of the mind-body problem (late 18th century) Dualism (Δυϊσμός) The mind and body are separate entities Monism (Μονισμός) The mind and body are one in the same Two types of monism: – Materialism – mental events are just a special kind of physical event – Subjective idealism – physical events Rene Descartes (1596-1650) Body and mind as separate entities. The brain is physical. The mind is nonphysical. The mind is not subject to the forces that operate on the physical world, hence the idea of “the immortal soul” Mind controls the body’s higher functions, though some actions are independent and reflexive (e.g. digestion, respiration). Belief in free-will Psychologists argued against the dualist position. The mind and the physiology of the central nervous system are merely two aspects of the same process, two ways of explaining the same thing. Gilbert Ryle, (1949) described dualism as the “doctrine of the ghost in the machine” and criticized for invoking the idea of a “homunculus” in the head If we believe that the nervous system is a biological machine subject to the laws of nature, then so is the mind (Mechanistic view) The Rise of Behaviourism - B.F. Skinner Behaviour can be researched scientifically without recourse to inner mental states (since cannot be observed) Human behaviour is reducible to conditioned associations, repertoires of learned responses Free will is an illusion Behaviourism was the dominant school in psychology for about 40 years until the 1950s, when the advent of computers gave us a new model of the mind. The Rise of Cognitivism Mental processes can be observed indirectly, through making inferences from performance in experimental tasks (such as reaction times and errors) and through self-reports. What is happening in the “black box” in our head when we see, hear, recognize objects & how we generalise from experience point to the conclusion that the mind uses mental representations or symbols (Pinker, 1997) The development of computer technology in the 1950s gave scientists a new metaphor for the mind. There is a symbolic code (or language) that the mind uses to represent information. Information processing is the encoding and re-encoding of information through a series of stages to extract different aspects of the information. The mind is not a single organ, but a system of organs which we can think of as psychological faculties or mental modules (Pinker, 1997) Mental modules are not likely to be visible, circumscribed territories – they may sprawl across the brain as distributed Subsystems or they might be broken down into regions that are connected by fibers that make the region act as a unit.
Classical computational models do not resemble underlying brain structures (there are no little boxes in the head)! They also tend to be rule based and use serial processing.
“Connectionism” An alternative to the classical computational approach comes from cognitive science – a multidisciplinary field closely aligned to the study of artificial intelligence (AI). Connectionist models aim to resemble neurological structures mental events can be described by interconnected networks of simple units at any time a unit in the network has an activation level, which is a numerical number intended to represend some aspect of the unit Connectionist models incorporate the notion of spreading activation. Over time a unit's activation spreads to all the other units connected to it the sum of activation is how things are represented in the brain – no symbol system Neural networks and biological realism: WHERE DO WE STAND Taking inspiration from natural systems rather than artificial (not the computer, but the brain itself – neurons and synapses) units in a connectionist network could represent neurons and the connections could represent synapses if the units in the model are neurons, the activation could represent the probability that the neuron would generate an action potential (be active in the network)
So where are psychobiologists and cognitive psychologists at today?
Biological and cognitive psychologists tend to be methodological materialists, that is, they go about their work assuming that mental states have physical causes. That is not to say that mental states are simply the resultof physical causes and we don’t have a choice. So free will or determinism? Pinker (1997) and others suggest it is a false dichotomy. We should believe that we have free will when we act and make moral judgments in the real world. But when, as scientists, we are trying to systematically explain and predict behaviour we need to assume that everything has a cause and can be predicted.
Lecture 2 - Anatomy of Neuron
Part II: Neuron Human brain made of 1012 neurons (10.000.000.000.000) The nervous system consists of two types of cells •Neurons - receive information and transmit them to other cells •Glia (neuroglia) exchange chemicals with adjacent neurons.
Outside the Neuron
Inside the Neuron…
Cell Membrane •2 layers of fat molecules •Embedded within are proteins •Channel proteins: transport other molecules through •Signal proteins: transfer a signal inside of neuron when molecules attach Supportive Cells •CNS: glia cells (in the PNS we have the satellite cells) •Provide physical and functional support •Form a physical matrix that “glues” neural circuits together (glia means glue) •Absorb dead cells Glial Cells: Astroglia/Astrocytes Astrocytes help synchronise the activity of the axon Oligodendrocytes/Schwann cells build myelin sheaths that insulate axons Radial glia provides guidance during embryonic development Myelination • Myelin: fatty insulating substance • Myelin sheets increase speed & efficiency of axonal conductance • Each Schwann cell constitutes 1 myelin segment; each oligodendroglia cell constitutes several segments • Only Schwann cells can guide axonal regeneration • Myelin-related diseases: e.g. Multiple Sclerosis (MS)
Lecture 3 - Biological Bases of Behaviour
Part I: General Brain Anatomy Two Major Divisions •Central Nervous System (CNS) located in skull and spine CNS = brain + spinal cord •Peripheral Nervous System (PNS) outside skull and spine PNS = Somatic NS + Autonomic NS
Somatic: interacts with environment Afferent (incoming) sensory nerves Efferent (outgoing) motor nerves Autonomic: regulation of internal environment Afferent and efferent nerves to and from internal organs
Autonomic nervous system 2 kinds of efferent nerves: Sympathetic nerves: Project from CNS in lumbar and thoracic regions of spine Parasympathetic nerves: Project from brain and sacral region of spine Both symp & parasymp nerves project to second-stage neurons, then to organs
Symp vs. Parasymp
1. Sympathetic nerves stimulate, organize and mobilize energy resources in threatening situations Parasympathic nerves conserve energy 2. Each organ receives opposing input from both, so a balance is struck between the two: 3. Sympathetic arousal, Parasympathetic relaxation e.g. heart: symp increase heart rate, parasymp decrease heart rate
According to MacLean (1952) the human brain can be regarded as having 3 evolutionary distinct parts. •THE REPTILIAN BRAIN. Composed mainly of the brainstem and basal ganglia. It mediates basic reflexes necessary for life. •THE OLD MAMMALIAN BRAIN. Composed mainly of the limbic system and is involved in emotion. •THE NEW MAMMALIAN BRAIN. Represented by the cerebral cortex which reaches its greatest complexity in man. It is involved in language, thought and consciousness Brain Development •Nervous system develops from embryonic tissue called the ectoderm •First sign: neural plate appears at day 20 •Next day: neural groove formation •Day 21: edges meet to form the neural tube •Day 24: differentiation
5 Divisions of the Brain
I ) Telencephalon: Cerebrum Cerebral cortex is greatly convoluted – leading to enlargement of surface •Gray matter: neurons & glia •White matter: axons that connect the neurons of cerebral cortex with those located elsewhere in brain Sulcus: small groove Fissure: large groove Gyrus: convolution separated by sulci or fissures Cerebral Cortex divided into four areas or lobes: Frontal lobe (the “front”) includes everything in front of the central fissure Parietal lobe (the “wall”) is located on the side of the hemisphere, just behind the central fissure Temporal lobe (the “temple”), at the base of the brain, ventral to the frontal and parietal lobe) Occipital lobe lies at the very end of the brain, caudal to parietal and temporal lobes Cerebral Cortex: Functional Anatomy Three areas of the cerebral cortex receive info from sensory organs: primary visual cortex, primary auditory cortex, primary somatosensory cortex •One area controls movement: primary motor cortex •Note: All connections are contralateral – the left hemisphere controls the right side of body and vice versa •80% serves to associate info needed for memory, learning etc I) Telencephalon: Limbic Cortex •The limbic cortex is another form of the cerebral cortex •Located around the medial edge of the cerebral hemispheres (limbus means “border”) •Cingulate (“circling”) gyrus the most prominent structure •Component of the “Limbic System” Limbic System. Papez (1937): A set of interconnected brain structures, including the limbic cortex, control motivation and emotion Mc Lean (1949): term “limbic system” consisting of limbic cortex hippocampus (“sea horse”) and amygdala (“almond”) in temporal lobe Fornix (a bundle of fibres linking the hippocampus to mammillary bodies of hypothalamus) Mc Lean (1949): evolution of the limbic system appears to have coincided with the development of emotional responses Today: Hippocampal formation and limbic cortex: Learning and memory Amygdala specifically involved in emotion: Feelings & expressions of emotion Emotional memories Recognition of the signs of emotions in other people
The Basal Ganglia •Group of subcortical structures: Caudate nucleus, Putamen, Globus pallidus •Primary function: Control of movement •Basal ganglia interact with frontal cortex areas responsible for planning sequences of behaviour, certain aspects of memory and emotional expression •Prominent basal ganglia diseases: Parkinson’s and Huntington’s disease The Basal Forebrain •Several structures including the Nucleus basalis of Meynert •Receives input from basal ganglia and hypothalamus and projects to widespread areas of cortex (Acetylcholine) •Nucleus basalis is key part of the brain’s system for arousal, wakefulness, attention •Patients with Alzheimer’s and Parkinson’s disease have impairment in attention and intellect because of reduced nucleus basalis functioning
II) The Diencephalon
•Diencephalon is situated between the telencephalon and the mesencephalon •Its most prominent structures are: Thalamus Thalamus (from the Greek thalamos, “inner chamber”) 1. Constitutes the top of the brainstem 2. Located in the centre of the forebrain 3. Two-lobed structure Most sensory information goes first to the thalamus for processing and integration Thalamus sends output to specific regions of the cerebral cortex Thalamus = relay station =“Gate to Consciousness” Exception: old factory information which is transferred directly to cerebral cortex Thalamus is divided into several nuclei: 1. Nuclei, which receive info from sensory systems and relay the info to specific sensory projection areas of the cortex (e.g. lateral geniculate body & dorsomedial nucleus) 2. Nuclei, which relay motor information (e.g. ventral lateral nucleus) 3. Nuclei, which control cortex excitability with widespread projections to all cortical regions ( important for Arousal, Sleep…) Hypothalamus Hypothalamus (hypo means “below”) 1. Located just below the anterior thalamus 2. Small structure, but a very important one… Lies at the base of the brain, under the thalamus Controls the autonomic nervous system and the endocrine system (hormones) Organizes behaviour related to survival of the species – the so called four F’s: fighting, feeding, fleeing, and mating The hypothalamus contains a number of distinct nuclei 1. It controls (through nerves/trough hormones) the activity of the pituitary gland (“master gland”) 2. Damage to certain hypothalamic nuclei leads to abnormalities in motivated behaviours such as: Feeding and drinking Temperature regulation Sexual behaviour Activity levels It attracts great deal of research interest
Pituitary Gland •Pituitary gland is an endocrine (hormone-producing) gland •Attached to the base of the hypothalamus by a stalk that contains neurons, blood vessels and connective tissue •In response to messages from the hypothalamus, it synthesizes and releases hormones into bloodstream, which carries them to other organs
III) Midbrain: The Mesencephalon
Its most prominent structures are: Tectum (roof) Tegmentum (covering)
The tectum (“roof”) is the dorsal surface of the midbrain •Composed of 2 pairs of bumps, the colliculi (“little hills”): Superior colliculi - Part of the visual system; control visual reflexes and reactions to moving stimuli Inferior colliculi - Part of the auditory system
•The tegmentum (“covering”) lies beneath the tectum •Composed of: Periaqueductal gray –Implicated in pain control –Mediates the analgesic (pain-reducing) effects of opiates Red nucleus –Relays motor info from the cortex and cerebellum to spinal cord Substantia nigra (“black substance”) –Projects to the basal ganglia –Degeneration causes Parkinson’s disease
I. Medulla oblongata •Medulla oblongata (“oblong marrow”) is the most caudal portion of brain stem, just above spinal cord •Origin of several cranial nerves •Controls a number of vital reflexes: –Breathing, heart rate, vomiting, salivation, sneezing… •Damage to medulla is fatal, also large doses of opiates because they strongly suppress activity in medulla II. Cerebellum •The cerebellum (“little brain”) is located dorsal to the pons •Has 2 hemispheres, is a miniature version of the cerebrum (covered by cerebellar cortex, set of nuclei deep inside) •Proposed functions: –Control of movement: balance and coordination –Shifting attention between auditory and visual stimuli –Timing (e.g. tapping a steady rhythm; determining whether one rhythm is faster than another etc.)
III. Pons •The pons (“bridge”) lies between the mesencephalon and medulla •Contains some nuclei for cranial nerves (e.g. V= trigeminal nerve) •Contains major parts of the reticular formation –Netlike (reticulum means “little net”) structure with ascending and descending portions –Descending portion: controls motor areas of spinal cord –Ascending fibres: innervate the whole cortex increasing arousal and attention
Part II: Neuronal Communication The transmission of information within and between neurons is a complicated mix of: I) Electrical (within the neuron) II) Chemical (between neurons)
Brain is a finely tuned electrochemical organ.Blood-brain barrier blocks passage of many (toxic) chemicals from blood to brain. Not all molecules are blocked – some (e.g. glucose) are actively transported through the vessel walls. Others are allowed to pass but only in certain brain areas – e.g. sex hormones, stress hormones.
I ) Electrical Communication: John Z. Young (1936) discovered the largest axon located in a squid (1mm diameter> 100 to 1000 times larger than of a typical mammalian axon) Hodgkin & Huxley (1952): placed electrodes in the neuron & recorded the electric charge measured between the inside (intracellular) and outside (extracellular) of the cell membrane. This voltage difference when the cell is not transmitting an electrical impulse was named the Resting Membrane potential (RMP)= -70 millivolts (mV). In this ” resting” state a neuron is considered to be polarized. Different concentration of Ions inside & outside of the neuron. Ions are positively (+) or negatively (-) charged particles (atoms). The interior of a neuron is negatively charged compared with its outside. Ions include: Sodium Na+ (Latin Natrium) & Chloride Cl- Potassium K+ (Latin Kalium) Na+ highly concentrated outside the cell (14:1 ratio) Same are Cl- ions (25:1 ratio) K+ highly concentrated inside the cell (28:1 ratio), with other proteins We know that uncharged molecules (e.g. water) pass freely a cell’s membrane
Due to the uneven distribution of ions how does the neuron maintain its Resting Membrane potential (RMP)? Factors that contribute are: random motion selective membrane permeability sodium potassium pump a) Random motion & Concentration gradient: molecules are in constant random motion tending to an even distribution along the neural tissue. This motion results ions to concentrate from regions of high concentration to those of low concentration. –High [K+] 20 times more inside –High [Na+] 10 times more outside b) Electrostatic Pressure Ions (positive or negative) are dispersed continuously due to the same or opposite charging
c) Sodium Potassium Pump energy consuming mechanism (20% of cell’s energy spent) K+ and Cl- pass through the membrane with ease Na+ & negatively charged proteins very difficult (if not impossible) It forces out approximately 3 Na+ for every 2 K+ it takes back in!
Postsynaptic Action Potentials
A variety of signals arrive at the dendrites & set off a wave of electrical activity which passes through the cell body and to the axon. If this stimulation makes the voltage inside the cell positive, (depolarises the receptive membrane) & is called Excitatory Postsynaptic potentials (EPSPs) -Increase the likelihood that the neuron will fire (Action Potential)
Nodes of Ranvier
Increase of speed node to node jumps are passive ions exchange here Renewal of AP When axon hillock potential reaches -55mV triggers an AP AP is an ‘all-or-none response’. Either occurs to the full extent or not. A variety of signals arrives at the dendrites & set off a wave of electrical activity which passes through the cell body and to the axon. If this stimulation makes the voltage inside the cell negative, (hyperpolarises the receptive membrane) & is called Inhibitory postsynaptic potentials (IPSPs) – Decrease the likelihood that the neuron will fire IMPORTANT: The Refractory period The AP takes place over ms After that there is an •Absolute refractory period For 1-2ms after an AP that a second one it cannot be elicited followed by a •Relative refractory period only if signal is of higher intensity will the neuron fire II) Neuronal Communication The transmission of information between neurons is a –chemical process Otto Loewi (1921) discovered the chemical transmission of the nervous impulse during his sleep!! Used the hearts of frogs (excited as ours by sympathetic & parasympathetic nerves) • stimulated the vagus of the intact heart-slowed down the beat • placed the fluid into the recipient heart- Same result! Concluded that the chemical released in the fluid by the vagus
The Synapse in detail
The gap (tiny fluid space – 0.00002mm) between the terminal button of one neuron and the membrane of another
Synapses can occur in 3 places: on dendrites (axodendritic), somas (axosomatic), axons (axoaxonic) Axodendritic synapses are on the smooth surface of a dendrite (a) or on dendritic spines (b)
Details of Synapses •Presynaptic membrane at the end of the terminal button •Postsynaptic membrane located on neuron that receives the message (postsynaptic neuron) •Synaptic cleft is the space between presynaptic and postsynaptic membranes –Around 20 nm wide (1 nm = one-billionth of a meter) –Contains extracellular fluid, neurotransmitter diffusion In the terminal buttons: •Mitochondria: implies that the terminal button needs energy •Synaptic vesicles: (“little bladder”) contain few hundred molecules of a neurotransmitter •Golgi complex: produces some of the synaptic vesicles (The others are produced in the cell soma & transported to the terminal button) Directed vs. non-directed Synapses •Directed synapses: site of neurotransmitter release and site of reception are in close proximity – Neurotransmission • Nondirected synapses: site of neurotransmitter release is at some distance from the site of reception - Neuromodulation
Processes during the Chemical transmission a)The axon terminals of the presynaptic neuron receive an electrical impulse (i.e. Action Potential) and as a result they release chemicals called Neurotransmitters that b) travel across the synapse, and c) act on the postsynaptic neuron at sites called receptors, d) this activation either increases or decreases the resting voltage of that neuron. If the neuron is excited past a level at its axon hillock, it then, e) generates an electric signal that is passed down its axon leading to neurotransmitter release, & the whole process begins again.
Action potential stimulates influx of Calcium ions & the synaptic vesicles fuse with the presynaptic membrane, spilling their contents into the synaptic gap.
This spilling of neurotransmitter from presynaptic neuron is called Exocytosis.
Termination of synaptic transmission To avoid continual action of the neurotransmitter the message has to be terminated Two mechanisms –Re-uptake –Enzymatic degradation Neurotransmitter Deactivation •Prevents ‘clogging’ of communication •2 mechanisms: –Reuptake: neurotransmitters drawn back into presynaptic buttons & repackaged in vesicles –Enzymatic degradation: broken apart in synaptic cleft by enzymes (e.g. acetylcholinesterase breaks down acetylcholine)
Each receptor only “accepts” a certain neurotransmitter One neurotransmitter may bind to different receptors (receptor subtypes) The membrane of the nerve cell contains 2 types of ion channel: Receptors: The Ionotropic One Ligand-activated ion channels opened by neurotransmitters which produce tiny voltage changes known as excitatory or inhibitory postsynaptic potentials (EPSPS or IPSPs). VOLTAGE GATED which are opened by voltage changes inside the neuron and are responsible for the action potential. The Metabotropic Ones More prevalent Effects are slower to develop & more long lasting, diffuse, & varied. Trigger the ‘Second Messenger’: Influence genetic expression. Signal proteins & G proteins (guanosine-triphosphate-sensitive proteins) The Metabotropic Ones a) Autoreceptors
Heteroceptors •Located presynaptically •modulates release of neurotransmitter •respond to different neurons
Neurotransmitter Molecules: The small and the large ones
Produced in the cytoplasm of button •Packed in synaptic vesicles by Golgi complex (cisterna) •Stored until released into synaptic cleft Synthesis •Transmitter is made from a precursor molecule •this molecule is adapted by the presence of enzymes •different transmitters have different synthesis FOUR types of Neurotransmitters 1)Amino acids Glutamate –most prevalent excitatory transmitter in the brain & spinal cord •Aspartate •Glycine appears to be the inhibitory neurotransmitter in the spinal cord and lower portions of the brain. •gamma-aminobutyric acid [GABA] –most prevalent inhibitory transmitter in the CNS
2)Monoamines Synthesized from a single amino acid (mono) •Effects more diffuse than amino acid neurotransmitters •Mostly operate in cells located in brain stem •Neurons often have highly branched axons with many varicosities •Monoamines diffusely released (‘volume transmission’) a) Catecholamines I. Dopamine DA Mesostriatal pathway: maintaining normal motor behaviour loss of dopamine >> Parkinson’s disease Mesolimbocortical pathway: Part of the brain’s reinforcement system Increased dopamine >> Schizophrenia II. Noradrenaline (norepinephrine) NA Part of the brain’s activation system –Arousal, attention sleep etc. •Emotional tone –Decrease >> depression –Increase >> mania (overexcited behaviour) Noradrenaline (norepinephrine) NA Tends to be excitatory in the ANS III. Adrenaline (epinephrine) N •Important in arousal •adrenaline prepares the body for: –fast dramatic action –speeding heart rate –increasing the blood supply to the muscles –restricting the blood supply to the digestive system
b) Indolamine Serotonin (5-HT) - Important in mood and emotion, regulation of sleep, biological cycles Low levels of serotonin in the brain associated to behaviours such as: depressions suicide impulsive aggression alcoholism explosive rage High levels of serotonin have been associated with: obsessive compulsion Fearfulness lack of self confidence shyness 3)Soluble gases Recently discovered class of neurotransmitters •Nitric oxide & Carbon monoxide –Produced in the neural cytoplasm –Diffuse through cell membrane and then into the nearby cells –Easily pass through membranes Two proposed functions:
1. Stimulate production of second messenger 2. Retrograde signalling: information feedback from the postsynaptic membrane to the presynaptic one 4)Acetylcholine In a class of its own Small-molecule neurotransmitter All muscular movement is accomplished by the release of acetylcholine. Possibly the most widely used neurotransmitter in the body and all axons that leave the central nervous system e.g. those running to skeletal muscle or to sympathetic or parasympathetic ganglia use actylcholine as their neurotransmitter. Neurons releasing acetylcholine are called cholinergic neurons Found in high concentrations in the limbic system. Regulation of the waking state, attention •Important for learning & memory processes •Hypothesis: –Death of acetylcholine neurons in basal forebrain >> decrease of acetylcholine in neocortex >> memory deficits in Alzheimer’s disease (?)
Produced by protein-biosynthesis in cell body (ribosomes involved) •Packed into vesicles by cell body’s Golgi complex •Transported to button by microtubules A transmitter can be excitatory inhibitory increase or decrease likelihood of AP.
Behaviours Associated with Neurotransmitters Transmitter associated behaviours dopamine symptoms of schizophrenia Serotonin symptoms of depression noradrenalin symptoms of depression acetylcholine motor control Endorphins pain modulation GABA symptoms of anxiety disorders
Lecture 4 – Vision From the eye to the brain
Light Light is thought of in two different ways: • a continuous WAVE with a particular frequency OR •as discrete particles of energy –photons- travelling through space at about 300,000 km/sec that are between 380-760 nanometres in length called the human visual spectrum. The qualities of light we perceive are: Colour Brightness Perception of an object is a matter of how much light is absorbed & reflected from its surface….
Cross-section of the vertebrate eye
Iris (ίριδα): regulates how much light will reach the retinas.. Pupil (κόρη): hole in iris from which the light enters Lens (φακός): focuses incoming light on the retina Retina (αμφιβληστροειδής): 250 μm size of a razor blade edge contains photoreceptors Much of neural processing occurs at the retina from - 125 million rods (dim light)-the scotopic system –6 million cones (colour and bright light)- the photopic system
ODD system?? The incoming light must pass through the overlying cell layers before reaching the receptors. Yet, there is NO distortion….
Where the axons of retinal ganglion cells penetrate the retina and exit the eye has no receptors thus creating a blind spot The visual system uses visual information gathered from receptors around the optic disk to "complete" the visual image. Distortion of incoming light is minimized by the Fovea (contains only cones) an indentation, about 0.33 centimetre in diameter, allows high acuity vision. Convergence of neural input occurs between the photoreceptors & each ganglion cell. –Several hundred rods may converge to a single ganglion cell. This analogy diminishes towards the center of the retina. In fovea a ganglion cell may receive input from just a few cones
Cones (center of retina) Bright light vision –normal daylight vision Good visual acuity Foveal vision Low convergence Colour vision
Rods (periphery of retina) Dim light vision Poor visual acuity; achromatic High convergence Movement detection
II ) Visual pathways to the brain Retina Optic nerve Optic chiasm Lateral Geniculate Nuclei of the thalamus (LGN) [80% of axons terminate here-rest to Superior colliculus & Tectum] Primary visual cortex (striate cortex)
Contralateral – axons from nasal site of retina cross over Ipsilateral - temporal axons from retina remain to the same side of brain.
Lateral Geniculate Nuclei (LGN)
•Thalamic structure •Has 6 layers that receive information from both eyes. •Each layer of the pathway is organised like a map of the retina (retinotropic) •Optic fibres project to the primary visual cortex at the occipital lobe
Parvocellular layer (Small cell bodies) o Top 4 layers of LGN o Input from cones o Responsive to colour, fine pattern details, & to stationary or slowly moving objects
Magnocellular layer (Large cell bodies) •Bottom 2 layers of LGN •Respond to light of any wavelength •Analysis of moving objects
Primary Visual area (V1) 1.5mm thick Composed of Six layers Axons terminate in layer 4 (subdivided to 4a, 4b, 4Ca & 4Cb) 4b is striped- called striate cortex Input from both eyes converge in layer 4, enabling binocular analysis.
Striate Cortex Visual cortex has topographic organisation: Damage to small areas of visual cortex leads to blindness for the corresponding part of the visual field called ‘hemianopia’. 25% of visual cortex devoted to the analysis of foveal information. Receptive field Complex Cells common cells in striate cortex more numerous than simple cells have rectangular receptive fields respond to straight lines in specific orientation “that region of retina that, when stimulated, influences the firing rate of the neuron” Hypercomplex cells are similar to complex deal with lines of a particular length cells respond best to corners. Signals flow simple cells to complex cells •Visual Cortex neurons arranged in vertical columns•blocks within columns specialised for straight line of a particular orientation.
Kuffler (1953) Receptive Fields of ganglion cells
On-center cell fires when light hits its center (is also inhibited by light falling in the outer rim of the visual field) Off-center cell inhibited by light falling in the centre of the visual field, excited by light falling on the outer rim
Hubel and Wiesel (1950s to 1970s)
recorded the responses of single neurons in LGN & visual cortex of cats when viewing different types of visual stimuli won the Nobel Prize for Physiology & Medicine 1981
Hubel and Wiesel placed the tip of a microelectrode at Layer 4 of the visual cortex.
• The majority of striate cells have “on” and “off” zones • the on/off boarder is a straight line • Named simple cells.
Lecture 5 - Vision continued
Seeing Color To a large degree, the perception of an object's color depends on the wavelengths of light that it reflects into the eye. Sunlight and most sources of artificial light contain complex mixtures of most visible wavelengths. Creating Color experience Our experience of color is created by the nervous system Color is the brain’s way of letting us know which wavelengths are present. Information about the wavelengths that are reflected from objects is coded in neural impulses in the retina Then this information is transformed into the experience of color in the cortex What are some functions of color vision? 1. Ability to identify & classify things 2. Ability to tell one object from another 3. Ability to see objects against a varied background Trichromatic Theory of Color Vision also called Component theory First proposed in 1802 by Thomas Young (long before cones were discovered) Refined by von Helmholtz in 1852. “there are three different kinds of color receptors (cones), each with a different spectral sensitivity, and the color of a particular stimulus is presumed to be encoded by the ratio of activity in the three kinds of receptors” So, perception of color is the result of mixture of the 3 basic colors
Trichromatic theory could not explain the effect of negative after-image…. the afterimage produced by staring at: a red square is green and vice versa, While staring at a blue square is yellow and vice versa A black one gives a white effect Observed in color blindness where people cannot see red-green (very rare the blue-yellow) So then how can we explain the perception of yellow?? Opponent-Process Theory of Color Vision first proposed by Hering in 1878 Argued that yellow is also a primary color (not a mixture of red-green) . Hering argued for two types of color detector : Red-green Blue-yellow Black-white but acted to oppose each other Ganglion cells found to produce opposite responses: (De Valois & DeValois, 1988) a class of color-coding cells excited by red and inhibited red's complementary color*, green. 2.a class of color-coding cells was hypothesized to signal blue and its complement*, yellow, in the same opponent fashion 3.a class of brightness-coding cells was hypothesized to similarly signal both black & white. *Complementary colors are pairs of colors that produce white or gray when combined in equal measure (e.g., green light and red light).
Cortical Color Blindness (cerebral achromatopsia) Caused by: Brain injury Stroke Cone function is normal (receptors work) Color vision is lost Case study (M.S.) - No color perception •Could detect the border between two adjacent fields with different wavelengths even though both appeared the same shade of gray. The wavelength information is being processed by the undamaged area of the brain but the information is not being transformed into the experience of color due to damage to another area
Where is the object Fast response Reaching/grasping What is the object Slow response High acuity vision
Lecture 6 - Language in the Brain
Cerebrovascular Accidents (Strokes) Although the brain only makes up about 2% of body weight, it receives about 15-20% of its blood supply (The blood flow of the brain is about 750ml, or 1.5 pints, per minute). There are 2 types of stroke: a blood clot in the brain or neck (this is called a thrombosis) a blood clot from somewhere else that has moved and now blocks a blood vessel in the brain or neck (this is called an embolism) constriction or narrowing of an artery in the head or neck (this is called a stenosis) Haemorrhage. A rupture of a blood vessel. Stokes are the third most common form of death. The chances of one before 70 is about 1 in 20 (5%)
Brain damage & language impairment
Early reports: Aphasia refers to "partial or total loss of the ability to articulate ideas... due to brain damage." In 1836, Max Dax described 3 patients with language problems who all had left-sided frontal lobe damage. In 1861, Simon Aubertin stopped speech is a brain damaged man by pressing a spatula against the frontal lobes! Phrenology: Viennese physician Franz-Joseph Gall (1758-1828) Phrenologists attempted to label mental faculties (e.g.’mirthfulness’, sublimity’, conjugality’) located in brain “organs” on the surface of the brain detectable by looking at the skull. BUT complex mental processes are not located in small brain areas. Rather, brain areas have specific functions that contribute to and build up more complex processes.
Paul Broca (1861) French neurologist We have the beginning of the systematic study of the brain’s language system
observed a patient who following a series of strokes, was only able to utter the nonsense word “tan”, but could understand what was spoken to him. post-mortem autopsy revealed damage to the left inferior frontal area
Broca’s Aphasia (or Non-fluent aphasia) Patient is asked to describe the picture..... Symptoms: Speech production is slow Telegraphic speech, lacking in grammatical structure Difficulty in finding the “right word”, anomia. Patients with restricted lesions retain the ability to produce some sounds but show paraphasia Speech comprehension appears intact! Broca’s Aphasia Also called Motor Aphasia • difficulty producing an oral command “lick your lips” but intact self-generated licking after eating a doghnut
Wernicke’s Aphasia (or Receptive Aphasia) Symptoms: Their speech appears intact, is fluent but unintelligible Profound deficit in speech comprehension Carl Wernicke (1848-1905) German neurologist Damage appears on the left side of the brain at the posterior temporal cortex, adjacent to the primary auditory cortex
•Paraphasias – sound and/or word substitutions (e.g. “girl”-> curl, & “bread”-> cake) •Neologisms- say words that do not exist Also might present with anomia difficulty in naming persons or objects. •Reading & writing are also impaired. •Comprehension problems. The aphasic does not realise that their speech is meaningless – nor do they not realise they do not fully understand others. Wernicke’s area – stores the memories of word sound
Alexia & Agraphia In 1892, the French Neurologist Jules Dejerine reported the case of a patient called “Monsieur S” who awoke one morning to realise he could not read (Alexia). He was unable to recognise letters, or words, or write to dictation (Agraphia). However, he had no problem recognising objects or other people. Autopsy revealed damage to the Angular gyrus
Wernicke–Geschwind Connectionist Model of Aphasia
Conduction Aphasia This occurs when the pathway between Wernicke’s area and Broca’s area called the Arcuate fasciculus is damaged. •Speech is fluent and comprehension good. However, there is a problem in repeating words or phrases. •Geschwind (1965) showed that these types of aphasics can generally repeat concrete words (e.g. “house”), but not abstract ones (e.g. “abode”).
Localisation of function …….
Wada test : used to assess which hemisphere dominant for language (Wada & Rasmussen, 1960) • Injection of short-acting sodium amytal into left carotid artery first and then to the right leads to anaesthetisation of one hemisphere for c. 10 mins. Rasmussen and Milner (1977) tested 262 right hander found that 92% of right-handers had language lateralised in the lefthemisphere. But, for left-handers, this figure dropped to 70%.
Scanning the brain - Development of techniques
• The absorption of x-rays is correlated with tissue density, so can visualise skull, versus brain tissue, versus ventricles (or introduce dense material, e.g. angiogram) BUT • Conventional x-rays compress 3D structures into 2D Computerised Axial Tomography (CAT) scan built up from x-ray pictures taken at many angles Sophisticated computing and mathematics is used to reconstruct images at any level or orientation through the brain to build up a 3D picture. Magnetic Resonance Imaging (MRI). Similar to CAT except magnetic waves are used. It can also be used to measure blood flow allowing “functional” pictures to be taken (fMRI).
Positron Emission Tomography (PET)
•A radioactive element, or isotope, is introduced into the blood stream • As radioactive substance decays, positrons are released • When a positron hits an electron, both are annihilated and 2 photons are released at 180 degrees from each other travelling at the speed of light Positron Emission Tomography (PET) The simultaneous arrival of the 2 photons is detected by the radiation detectors around the subjects head • PET cameras can view multiple slices through the brain • The most radioactive sites in the brain can then be found by sophisticated computing and mathematics
Lecture 6 – Memory
Memory refers to one of the following: the mental function of retaining info about stimuli, events, images, ideas, etc after the original stimuli are no longer present the hypothesised ‘storage system’ in the brain that holds the info the info so retained Memory processes are complex. Different memory tasks recruit different memory processes. Different regions of the brain process different aspects of memory. ‘Learning refers to the process by which experiences change our nervous system and hence our behaviour. We refer to these changes as memories’. (Carlson 1999). Experiences change the nervous system by altering neural circuits.
Karl Lashley ‘s two laws:
•principle of mass action (memories are stored diffusely throughout the cortex) •principle of equipotentiality (all parts of the association cortex played an equal role in storage) concluded that no single structure was crucial Criticisms of Lashley •(1) Many subcortical structures (e.g. Limbic system, basal ganglia etc) are now known to be involved in learning and memory. •(2) Maze learning probably involves the formation of many “complex” memories (visual, touch, olfactory etc). These memories may be “localised” but appear to be distributed. •(3) Lashley believed that learning arose through stimulus-responses reflexes (classical conditioning). This is now known to be far too simple!
Ivan Pavlov (1849-1936)
Simple learning •habituation - depressing of synaptic activity •sensitisation - increase in synaptic activity
Donald Hebb (1904-1985)
Hebb (1949) argued that memory must involve biological changes in neurons or their connections. ‘‘When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficacy, as one of the cells firing B, is increased’’ (p.62)
Neural Mechanisms of Memory
Hebb didn’t have the means to test his theory. Yet, his suggestion was appealing since was compatible with the idea of memories being distributed in the brain, & how neurons might encoded & stored memory. Structural changes in synapses could be a mechanism to store memories Changes involving neurotransmitter release or changes in receptor sensitivity. such changes include greater release of neurotransmitter molecules and/or greater effects when the receptor molecules become more numerous or more sensitive the result of such changes would be an increase in the size of the postsynaptic potential (PSP) A synapse that is “strengthened” as a result of learning was called a “Hebbian synapse”.
Evidence supporting Hebb comes from long term potentiation (Bliss and Lomo 1973) in which neurons show long lasting alterations in excitability following electrical stimulation.
Patient H.M. & the amnesic syndrome
HM reported by Scoville and Milner (1957) Bilateral removal of hippocampus and surrounding cortex, including the amygdala bilaterally to control for epilepsy. After the operation H.M. was left with profound anterograde amnesia - (an inability to remember anything new for any length of time). e.g. H.M. saw regularly Dr Milner for 40y but each time had to be reintroduced). H.M. - working memory was normal (e.g. digit span) also ability to use language and to know the meanings of works remained intact. H.M. unable to recall events that had occurred less than twelve years before his operation. H.M. was able to acquire information in his development of new motor skills. With practice he was able to improve his performance on tasks e.g. motor learning - learning to navigate his way through a finger maze plus the Tower of Hanoi but he was not able to recall having practised the tasks. H.M. symptoms following his operation provide the classic description of amnesiac syndrome: a profound anterograde amnesia a less profound retrograde amnesia a persevered capability to use and understand spoken and written language a preserved capacity for motor learning
Theories of Hippocampal function Milner (1966) believes that the hippocampus is involved in the consolidation of memory into long term storage. But, this does not explain why HM can perform certain tasks. Squire (1986) proposes that HM has a deficit in declarative memory (i.e. knowledge, images and thoughts that can be “declared” to consciousness), but not procedural memory (i.e. memory that is performed in the “actual-doing” of a task). The declarative/procedural difference is sometimes referred to as explicit and implicit memory. Sergi Korsakoff (1889) described an illness in chronic alcoholics which exhibits anterograde and retrograde memory loss, slowness of thought, and apathy. Traditionally, Korsakoff’s disease has been associated with damage to the mammillary bodies located close to the hypothalamus. More recently, damage has been found in the dorsomedial thalamus (DMT). The effects of DMT damage has also been described in amnesic patient NA (Squire and More 1979).