UNIVERSITY OF THE CORDILLERAS

College of Arts and Sciences

Psychology and Behavioral Science Department
Baguio City

P108: Physiological Psychology

Module 5: Brain Plasticity

I. TEACHING-LEARNING OUTCOMES

A. Teaching-Learning Outcomes

At the end of the lesson, the students are expected to:

1. Describe the phases of neurodevelopment.

2. Discuss the evolution in our thinking about the birth of new neurons in the adult
mammalian brain.
3. Identify the different types of brain tumors and other types of neurological
diseases.
4. Discuss the neural processes involved in learning, memory, and the types of
amnesia.

B. List of Topics

a. Phases of Neurodevelopment
b. 2. Neuroplasticity in Adults
c. 3. Brain Damage and Neuroplasticity
d. 4. Learning, Memory, and Amnesia

II. TEACHING-LEARNING ACTIVITIES (Lesson Proper)

BRAIN PLASTICITY: The brain is not a static network of interconnected elements, it is a

PLASTIC (changeable), living organ that continuously changes in response to its genetic
programs and environment.

I. NEURODEVELOPMENT

➢ Begins with a fertilized egg cell and ends with a functional adult brain

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A. FIVE PHASES OF NEURODEVELOPMENT

1. INDUCTION OF THE NEURAL PLATE

➢ Three weeks after conception, the NEURAL PLATE (a small patch of ectodermal
tissue of the dorsal surface of the embryo) becomes recognizable.
➢ The development of the neural plate is induced by chemical signals from the
underlying mesoderm.

➢ STEM CELLS
o Cells of the neural plate
o Have an unlimited capacity for self-renewal and have the ability to develop
many different kinds of cells.

2. NEURAL PROLIFERATION

➢ Once the lips of the neural groove fused to create the NEURAL TUBE, the cells of
the tube begin to PROLIFERATE (increase in number).
➢ Most cell division occur in the VENTRICULAR ZONE adjacent to the ventricle.
➢ In each species, the cells in different parts of the neural tube proliferate in a
particular sequence that is responsible for the pattern of swelling and folding that
gives the brain of each member of that species its characteristic shape.

3. MIGRATION AND AGGREGATION

➢ Once cells have been created through cell division in the ventricular zone, they
MIGRATE to the appropriate target location.
➢ The cells are still in an immature form, lacking the processes that characterize
mature neurons (axons and dendrites).
➢ In each region of the tube, subtypes of neurons arise on a precise and predictable
schedule and then migrate together to their prescribed destination.

➢ TYPES:

o RAIDAL MIGRATION
▪ Proceeds from the ventricular zone in a straight line outward toward the
outer wall of the tube.

o TANGENTIAL MIGRATION
▪ Occurs at a right angle to radial migration.

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 ➢ METHODS:

o SOMAL TRANSLOCATION
▪ An extension grows from the developed cell in the direction of the
migration and explores the immediate environment for attractive or
repulsive cues as it grows.

o GLIA-MEDIATED MIGRATION
▪ RADIAL GLIAL CELLS (a network of glial cells appear in the developing
neural tube).
▪ Many cells engaging in radial migration do so by moving along the radial
glial network.

➢ NEURAL CREST
o Structure dorsal to the neural tube formed by cells that break off from the
neural tube as it is being formed.
o Its cells develop into neurons and glial cells of the Peripheral Nervous System
as well as many other cell types in the body.

➢ AGGREGATION
o Once developed neurons have migrated, they align themselves with other
developing neurons that have migrated to the same area to form the structure
of the nervous system.
o Mediated by CELL-ADHESION MOLECULES located at the surface of neurons
and other cells; they have the ability to recognize molecules on other cells and
adhere to them.

4. AXON GROWTH AND SYNAPSE FORMATION

➢ Once neurons have migrated to their appropriate positions and aggregated into
neural structures, axons and dendrites begin to grow from them.
➢ SYNAPSE FORMATION occurs once axons have reached their intended sites and
have established an appropriate pattern of synapses.
➢ SYNAPTOGENESIS depends on the presence of glial cells (ASTROCYTES)
o Developing neurons need high levels of cholesterol during synapse formation
and extra cholesterol is supplied by astrocytes.

5. NEURON DEATH AND SYNAPSE REARRANGEMENT

➢ Neuron death is a normal part of development

➢ APOPTOSIS
o Active cell death where DNA and other internal structures are cleaved apart
and packaged in membranes before the cell breaks apart,
o Removes excess neurons in a safe, neat, and orderly way.

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 o Triggered by:
▪ Genetically programmed early neuronal death once they have fulfilled their
functions in the absence of external stimulus.
▪ Developing neurons seem to die because they fail to obtain the life-preserving
chemicals supplied by their targets.

➢ SYNAPSE ARRANGEMENT
o Cell death results in a massive rearrangement of synaptic connections
o Focus the output of each neuron on a smaller number of postsynaptic cells,
thus increasing the selectivity of transmission.

B. POSTNATAL GROWTH OF THE HUMAN BRAIN

➢ After birth, the human brain volume quadruples between birth and adulthood,
with much growth occurring in the first year and continuing into the third year.

➢ Brain growth is the result of:

o INCREASED LEVELS OF SYNAPTOGENESIS IN THE HUMAN CORTEX SHORTLY AFTER

BIRTH

▪ Postnatal formation of synapses indicates the brain’s analytic ability due to

the number of connections between neurons in a particular brain region.

▪ Differences of synaptogenesis among cortical regions:

• Primary Visual and Auditory Cortices: Synaptogenesis at 4 months and
maximum synapse density at 7 – 8 months.
• Prefrontal Cortex: Steady rate of synaptogenesis reaching maximum
synapse density in the second year.

o MYELINATION

▪ Myelination increases the speed of axonal conduction and myelination of

various areas of the human brain during development roughly parallels in
their functional development.
▪ Myelination at sensory areas occurs in the first few months followed by
myelination of the motor areas.
▪ Myelination of the prefrontal cortex continues until adulthood.

o DENDRITIC BRANCHING

▪ The process duplicates the original pattern of neural migration in the sense
that dendritic branching progresses from deeper to more superficial layers.

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C. DEVELOPMENT OF THE PREFRONTAL CORTEX (PFC)

➢ Functions of the PFC:

o Working Memory: Keeping relevant information accessible for short periods of

time while a task is being completed.
o Planning and carrying out sequences of action
o Inhibiting responses that are inappropriate in the current context but not in
others.
o Following rules of social behavior

➢ Jean Piaget’s Theory of Cognitive Development

o PERSEVERATION
▪ Tendency to continue making a formerly correct response when it is
currently incorrect.
▪ Observed between 7 – 12 months due to the immaturity of the PFC’s neural
circuitry and the synapse number do not reach its maximum level until the
second year.

II. NEUROPLATICITY IN ADULTS: NEUROGENESIS

➢ Neurogenesis in nonhuman adult mammals is restricted to the olfactory bulb and

hippocampus with low levels in the hypothalamus.

➢ In adults, it is observed in the STRIATUM and the HIPPOCAMPUS

o New hippocampal neurons have roles in memory function that facilitates
PATTERN SEPARATION, the ability to separate distinct percepts into individual
memories for storage.
o Adult hippocampal neurogenesis is found to play a role in mood and anxiety
regulation.

III. BRAIN DAMAGE AND NEUROPLASTICITY

A. CAUSES OF BRAIN DAMAGE

1. BRAIN TUMORS

➢ Mass of cells that grows independently of the rest of the body.

➢ 20% are MENINGIOMAS (tumors that grow between meninges).
➢ ENCAPSULATED TUMORS: Tumors that grow within their own membranes.
➢ INFILTRATING TUMORS: Grow diffusely through surrounding tissue.
o MALIGNANT TUMORS
▪ Difficult to remove or destroy

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 ▪ Cancerous tissue that remains after surgery continues to grow
▪ Example: GLIOMAS

o METASTATIC TUMORS
▪ Tumors that grow from infiltrating cells carried to the brain by the
bloodstream from other parts of the body.

2. CEREBROVASCULAR DISORDER: STROKES

➢ Strokes are sudden-onset cerebrovascular disorders that cause brain damage, the
symptoms depend on the affected area of the brain, but common consequences
are amnesia, aphasia, paralysis, & coma.
➢ INFARCT: Area of dead or dying tissue produced by a stroke.
➢ PENUMBRA: Surrounds the infarct, the tissue may recover or die in the ensuing days
depending on a variety of factors.
o The primary goal of treating the stroke is to save the penumbra.

➢ TYPES:

o CEREBRAL HEMORRHAGE: Occurs when a cerebral blood vessel ruptures and

blood seeps into the surrounding neural tissue and damages it.

o CEREBRAL ISCHEMIA: Disruption of the blood supply to an area of the brain.

▪ THROMBOSIS: Blood clot, fat, oil, air bubble, tumor cells, etc. that blocks the
flow of blood.
▪ EMBOLISM: Plug carried by the blood from a larger blood vessel where it
becomes lodged.
▪ ARTERIOSCLEROSIS: Walls of the blood vessel thickens and the channels
narrow as a result of fat deposits.

3. CLOSED-HEAD INJURIES

➢ CONTUSIONS: Closed-head injuries that involve damage to the cerebral

circulatory system.

➢ CONCUSSION: Diagnosis given when there is a disturbance of consciousness from

a blow to the head and there is no evidence of a contusion or other structural
damage.

➢ CHRONIC TRAUMATIC ENCEPHALOPATHY: Dementia (general intellectual

deterioration) and cerebral scarring observed in boxers, rugby players, American
football players, and other individuals who have experienced repeated
concussive or sub-concussive blows to the head.

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4. BRAIN INFECTIONS

➢ BACTERIAL INFECTIONS lead to the formation of cerebral abscesses.

o MENINGITIS: Inflammation of the meninges
o SYPHILIS: General Paresis (dementia and mental illness caused by the
infection).

➢ VIRAL INFECTIONS
o RABIES: Virus has a particular affinity for the nervous system
o MUMPS & HERPES: Viruses that can attack the nervous system but have no
affinity for it.

5. NEUROTOXINS

➢ Damage caused by exposure to any one of a given variety of toxic chemicals.

B. NEUROLOGICAL DISEASES

1. EPILEPSY/ SEIZURE DISORDERS

➢ A SEIZURE is a period of sudden, excessive activity of cerebral neurons

characterized by involuntary movements, changes in consciousness or both.

➢ Two Distinctions:

o PARTIAL vs. GENERALIZED

➢ PARTIAL SEIZURES
o Have a definite focus, or source of irritation: typically, a scarred region
caused by an old injury.
o The neurons that become involved in the seizure are restricted to a small
part of the brain.

➢ GENERALIZED SEIZURES
o Widespread, involving most of the brain
o In many cases they grow from a focus, but in some cases their origin is not
discovered.

o SIMPLE vs. COMPLEX

➢ SIMPLE PARTIAL SEIZURES

o Often cause changes in consciousness but do not cause loss of
consciousness.

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 ➢ COMPLEX PARTIAL SEIZURES
o Lead to loss of consciousness

➢ GRAND MAL SEIZURE

o The most severe form of seizure

o Generalized, and because it includes the motor systems of the brain, it is
accompanied by convulsions.
o Often, before having a grand mal seizure, a person has warning symptoms,
such as changes in mood or perhaps a few sudden jerks of muscular activity
on awakening.

o AURA:
▪ Occurs a few seconds before the seizure which may be presumably
caused by excitation of neurons surrounding a seizure focus.

2. PARKINSON’S DISEASE

➢ Caused by degeneration of the nigrostriatal system – the dopamine-secreting

neurons of the substantia nigra that send axons to the basal ganglia.

➢ The primary symptoms of Parkinson’s disease are muscular rigidity, slowness of

movement, a resting tremor, and postular instability.

➢ RESTING TREMOR, vibratory movements of the arms and hands that diminish
somewhat when the individual makes purposeful movements accompanied by
rigidity; the joints appear stiff.

➢ LEWY BODIES, abnormal circular structures found within the cytoplasm that have
a dense protein core, surrounded by a halo of radiating fibers.

3. HUNTINGTON’S DISEASE

➢ Caused by degeneration of the caudate nucleus and putamen, especially of

GABAergic and acetylcholinergic neurons.

➢ Causes uncontrollable ones, especially jerky limb movements; look like fragments
of purposeful movements but occur involuntarily.

➢ The disease is progressive and eventually causes death.

➢ The symptoms of Huntington’s disease usually begin in the thirties and forties but
can sometimes begin in the early twenties.

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 ➢ The first signs of neural degeneration occur in the putamen, in a specific group of
inhibitory control exerted on the premotor and supplementary motor areas of the
frontal cortex. Loss of this control leads to involuntary movements.

➢ A hereditary disorder caused by a dominant gene on chromosome 4.

➢ Normal huntingtin is found in the cytoplasm, where it apparently plays a role in

production of certain cell organelles.
o In cells of genetically altered HD mice that express long huntingtin and develop
a disorder that closely resembles Huntington’s disease, fragments of huntingtin
begin to accumulate in the nucleus, which apparently triggers the production
of caspase.

4. MULTIPLE SCLEROSIS

➢ Autoimmune demyelinating disease

➢ At scattered locations within the central nervous system, myelin sheaths are
attacked by the person’s immune system, leaving behind hard patches of debris
called SCLEROTIC PLAQUES.
➢ The normal transmission of neural messages through the demyelinated axons is
interrupted, because the damage occurs in white matter located throughout the
brain and spinal cord, a wide variety of neurological disorders are seen.

➢ Afflicts women somewhat more frequently than men, and the disorder usually
occurs in people in their late twenties or thirties.

➢ People who spend their childhood in places far from the equator are more likely
to come down with the disease than are those who live close to it. In addition,
people born during the late winter and early spring are at higher risk.

➢ Some disease contracted during a childhood spent in a region in which the virus
is prevalent causes the person’s immune system to attack his or her own myelin.

➢ A virus weakens the blood-brain barrier, allowing myelin protein into the general
circulation and sensitizing the immune system to it, or perhaps that virus attaches
itself to myelin.

5. ALZHEIMER’S DISEASE

➢ Several neurological disorders result in dementia, a deterioration of intellectual

abilities resulting from an organic brain disorder.

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 ➢ People may have difficulty remembering appointments and sometimes fail to
think of words or other people’s names.
➢ The memory deficit most critically involves recent events, and thus it resembles the
anterograde amnesia of Korsakoff’s syndrome.
➢ Produces severe degeneration of the hippocampus, entorhinal cortex, neocortex,
nucleus basalis, locus coeruleus, and raphe nuclei.

➢ The brains of the affected individuals contain many amyloid plaques, which
contain a core of misfolded long-term beta-amyloid protein surrounded by
degenerating axons and dendrites, and neurofibrillary tangles, composed of
dying neurons that contain intracellular accumulations of twisted filaments of TAU
PROTEIN.

➢ Hereditary forms of Alzheimer’s disease involve defective genes for the amyloid
precursor protein (APP), for secretases that cut APP into smaller pieces, or for
apolipoprotein E (apoE), a glycoprotein involved in transport of cholesterol and
the repair of cell membranes.

IV. LEARNING, MEMORY, AND AMNESIA

A. THE NATURE OF LEARNING

➢ LEARNING

▪ The process by which experiences change our nervous system and hence
our behavior in the form of memories.
▪ Experiences are not “stored”; rather, they change the way we perceive,
perform, think, and plan by physically changing the structure of the nervous
system, altering neural circuits that participate in perceiving, performing,
thinking, and planning.

➢ BASIC FORMS OF LEARNING

▪ PERCEPTUAL LEARNING
• The ability to learn to recognize stimuli that have been perceived
before.
• The primary function of this type of learning is the ability to identify
and categorize objects (including other members of our own
species) and situations.
• Each of the sensory systems is capable of perceptual learning.

▪ STIMULUS-RESPONSE LEARNING:
• The ability to learn to perform a particular behavior when a
particular stimulus is present.

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 • Involves the establishment of connections between circuits involved
in perception and those involved in movement.
• The behavior could be an automatic response such as a defensive
reflex, or it could be a complicated sequence of movements that
was learned previously.

▪ HEBB RULE
o If a synapse repeatedly becomes active at about the same time
that the postsynaptic neuron fires, changes will take place in the
structure or chemistry of the synapse that will strengthen it.
o If the 1000-Hz tone is presented first, then weak synapse T becomes
active. If the puff is presented immediately afterward, then strong
synapse P becomes active and makes the motor neuron fire.
o The act of firing then strengthens any synapse with the motor neuron
that has just been active.
o After several pairings of the two stimuli, and after several increments
of strengthening, synapse T becomes strong enough to cause the
motor neuron to fire by itself and learning has occurred.

B. LEARNING AND SYNAPTIC PLASTICITY

1. INDUCTION OF LONG-TERM POTENTIATION

▪ Electrical stimulation of circuits within the hippocampal formation can lead to

long-term synaptic changes that seem to be among those responsible for
learning.

▪ LONG-TERM POTENTIATION
▪ Increase in the magnitude of EPSP in the postsynaptic neurons due to
intense electrical stimulation of axons leading from the entorhinal cortex to
the dentate gyrus.

2. HIPPOCAMPAL FORMATION

o A specialized region of the limbic cortex located in the temporal lobe.

o The primary input to the hippocampal formation comes from the entorhinal
cortex.
o The axons of neurons in the entorhinal cortex pass thru the perforant path
and form synapses with the granule cells of the dentate gyrus.
o Long-term potentiation can be induced by stimulating the axons in the
perforant path with a burst of approximately 100 pulses of electrical
stimulation, delivered within a few seconds.

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 ▪ ASSOCIATED LONG-TERM POTENTIATION
o Long-term potentiation in hippocampal slices can follow the Hebb rule;
when weak and strong synapses to a single neuron are stimulated at
approximately the same time, the weak synapse is strengthened.

3. THE ROLE OF NMDA RECEPTORS

➢ Non-associative long-term potentiation requires some sort of additive

effect, a series of pulses delivered at a high rate all in one burst will produce
long-term potentiation, but the same number of pulses given at a slow rate
will not.

➢ NMDA (N-Methyl-D-Aspartate) RECEPTOR

▪ Plays a critical role in long-term potentiation

▪ Found in the hippocampal formation, especially in field CA1.
▪ Controls a calcium channel though it is normally blocked by a
magnesium ion (Mg2+), which prevents calcium ions from entering the
cell even when the receptor is stimulated by glutamate.
▪ If the postsynaptic membrane is depolarized, the Mg2+ is ejected from
the ion channel, and the channel is free to admit Ca2+ ions.
▪ Calcium ions enter the cells through the channels controlled by NMDA
receptors only when glutamate is present and when the postsynaptic
membrane is depolarized.
▪ The entry of calcium ions through the ion channels controlled by NMDA
receptors is an essential step in long-term potentiation.

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4. MECHANISMS OF SYNAPTIC PLASTICITY

➢ AMPA RECEPTORS

▪ Increase in the number of AMPA receptors strengthen an individual

synapse.
▪ Before long-term potentiation was induced, the AMPA receptors
clustered at the base of the dendritic spines but 15 minutes after the
induction of long-term potentiation, the AMPA receptors flooded into
the spines and moved to their tips – the location of the postsynaptic
membrane (Shi, et al., 1999)

▪ CaM-KII (Type II Calcium-Calmodulin Kinase)

• An enzyme present in dendritic spines that facilitate the entry of

calcium ions into the dendritic spines that caused AMPA receptors
to move into the postsynaptic membrane.
• A calcium-dependent enzyme, which is inactive until a calcium ion
binds with it and activates it.
• CaM-KII can bind with an intracellular component of the NMDA
receptor – and also with a set of linking proteins that can attach to
AMPA receptors which are then brought in vesicles to the
postsynaptic membrane of dendritic spines.

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 5. ALTERATION OF SYNAPTIC STRUCTURE

▪ Long-term potentiation increased the number of perforated synapses

formed with the presynaptic potentials. The presence of perforated
synapses appears to be one of the characteristic features of strengthened
synapses. (Geinisman, et al., 1991, 1996)

▪ PRESYNAPTIC CHANGES
• Production of Nitric Oxide in the dendritic spines in the hippocampal
formation, could diffuse only as far as the nearby terminal buttons,
where it might produce changes related to the induction of long-term
potentiation.

o LONG-LASTING LONG-TERM POTENTIATION

• Long-term potentiation that lasts more than a few hours – requires
protein synthesis.
• Drugs that blocks protein synthesis could block the establishment of
long-lasting long-term potentiation
o CA1 if administered before, during, or immediately after a
prolonged burst of stimulation was delivered, long-term potentiation
occurred, but it disappeared a few hours later. If administered one
hour after the synapses had been stimulated, the long-term
potentiation persisted.

C. AMNESIA

1. MEDIAL-TEMPORAL LOBE AMNESIA

➢ Preserved intellectual functioning and with evidence of medial temporal lobe

damage.
➢ Observed difficulty in forming explicit LTM while retaining the ability to form
implicit LTM with the same experiences.

2. AMNESIA OF KORSAKOFF’S SYNDROME

➢ Disorders of memory common in people who have consumed large amounts

of alcohol.
➢ Largely attributable to brain damage associated with Thiamine Deficiency
that accompanies alcohol consumption.
➢ Characterized by a variety of sensory and motor problems, extreme confusion,
personality changes, and a risk of death from liver, gastrointestinal, or heart
disorders.

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 ➢ Observed lesions to the medial diencephalon (thalamus and hypothalamus)
and diffused damage to several other brain structures neocortex,
hippocampus, and cerebellum.

3. AMNESIA OF ALZHEIMER’S DISEASE

➢ Memory deficits are more general and often display short-term memory
deficits and in verbal and perceptual implicit memory
➢ Low levels of acetylcholine results from the degeneration of the basal
forebrain.

4. POSTTRAUMATIC AMNESIA

➢ Anterograde memory deficits follow a nonpenetrating head injury

➢ RECONSOLIDATION: Each time memory is retrieved from long-term storage, it is
temporarily held in labile short-term memory where it becomes susceptible to
posttraumatic amnesia until it is reconsolidated.

D. AREAS OF THE BRAIN IMPLICATED IN MEMORY

1. INFEROTEMPORAL CORTEX

➢ Plays an important role in storing memories of visual input.

2. AMYGDALA

➢ Play a special role in memory for the emotional significance of experiences.

➢ Involved in strengthening emotionally significant memories stored in other
structures making emotion-provoking events easier to recall as compared to
neutral events.

3. PREFRONTAL CORTEX

➢ Implicated in two episodic memory abilities

➢ People with large prefrontal lesions display both anterograde and retrograde
deficits in memory for the temporal order of events, even when they can
remember the events for themselves.
➢ Deficits in working memory.

4. CEREBELLUM

➢ Storage of memories of learned sensorimotor skills through its various

neuroplastic mechanisms.

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 5. STRIATUM

➢ Store memories for consistent relationships between stimuli and responses

➢ Implicated in habit formation.

III. ANALYSIS/ ENHANCEMENT ACTIVITY: RESEARCH IN NEUROLOGY (30 POINTS)

INSTRUCTION: Choose one (1) cause of brain damage and complete the following table:
(Do not forget to indicate your references)

CAUSE OF BRAIN ASSOCIATED SPECIFIC BRAIN POSSIBLE

DAMAGE NEUROLOGICAL STRUCTURES/ AREAS TREATMENT/
DISORDER/S AFFECTED REHABILITATION

REFERENCES: (APA FORMAT)

REFERNECES:

Alila Medical Media (2017 April 4). Long term potentiation and memory formation,
animation. YouTube. Retrieved from
https://www.youtube.com/watch?v=4Hm08ksPtMo&ab_channel=AlilaMedicalMedia.

Carleton University (2013 November 7). Neuroscience – Long-term potentiation. YouTube,

Retrieved from
https://www.youtube.com/watch?v=vso9jgfpI_c&ab_channel=CarletonUniversity.

Carlson, N.R. (2005). Foundations of physiological psychology (6th Ed.). Boston, MA:
Pearson Education Inc., 356-397; 432-459.

Halo Neuroscience (2019 February 9). The neuroscience of learning. YouTube. Retrieved
from
https://www.youtube.com/watch?v=_nWMP68DqHE&ab_channel=HaloNeuroscience.

Pinel, J.P.J. & Barnes, S.J. (2018). Biopsychology (10 th Ed., Global Ed.). Essex, England: Pearson
Education Limited. 246-325.

TED-Ed (2014 August 26). What happens when you remove the hippocampus? – Sam
Kean. YouTube. Retrieved from
https://www.youtube.com/watch?v=KkaXNvzE4pk&ab_channel=TED-Ed.

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