Learning and memory functions are crucial in the interaction of an individual with the environment and involve the interplay of large, distributed brain networks. Recent advances in technologies to explore neurobiological correlates of neuropsychological paradigms have increased our knowledge about human learning and memory. In this chapter we first review and define memory and learning processes from a neuropsychological perspective. Then we provide some illustrations of how noninvasive brain stimulation can play a major role in the investigation of memory functions, as it can be used to identify cause–effect relationships and chronometric properties of neural processes underlying cognitive steps.

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2. LEARNING AND MEMORY
Learning-
Reflex Learning-
Non Associative-
Habituation
Sensitization
Associative-
Classical Conditioning
Operant Conditioning
Incidental Learning
Memory-
Physiologically On The Basis Of
How Information IsStored &
Recalled
Implicit Memory.
Procedural Memory
Priming
Explicit Memory
SemanticMemory
Episodic Memory
Depending Upon Permanency Of
Storage
Short Term.
Intermediate Long Term.
Long Term
Consolidation
Encoding
Retrieval
Applied Aspects
Substances Facilitate Memory And
Learning
Addiction
Amnesia
Antegrade
Retrograde
Senile Dementia
Alzheimer Disease
Concept Of DominantHemisphere

3. LEARNING & MEMORY
Learning – The ability to alter behavior on the
basis of experience.
Memory – Acquisition ,storage & retrieval of
sensory information. Ability to recall pastevents
at the conscious or unconscious level.
Thought – A thought result from a pattern of
stimulation of many parts of the nervous system
at the same time & in a definite sequence,
probably involving the cerebral cortex,thalamus,
limbic system, upper reticular formation of brain
stem.
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4. LEARNING .
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Reflex learning.
behavior change.
Incidental learning.
Associated with immediate Behavior change n
o
t
immediate
But person gets
information from
sensory inputs &
develop potential to
behave differently.
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5. REFLEX LEARNING.
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Non- associative .
Person learns about
properties of single
stimulus when repeatedly
exposed to same stimulus.
Associative.
Person learns about
relationship between two
stimuli or a stimulus &
behavior
.
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6. NON- ASSOCIATIVE.
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Habituation
Decrease in response to
benign stimulus when
stimulus presented
repeatedly.
Sensitization.
Increase in response to
benign stimulus when
stimulus presented
repeatedly with an
pleasant or unpleasant
stimuli.
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7. Habituation
Ifa stimulus is repeated
many times
First time it evokes a novel response (orientation
response or what is it response)
Evokes less & less response when repeated
Subject becomes habituated to the
stimulus & ignores it

8. Example
New clock in the room.
H8abituation
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9. Cellular basis of Habituation.
Given by KANDEL
& hiscolleague.
The brain learn to ignore matterof
less important.
This result from inhibition of the
synaptic pathway.
Repeated stimulus.
Gradual inactivation of Ca+
2
influx at axon endings.
Decrease intracellular Ca+2
Neurotransmitter release at
synapses.
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10. Sensitization
The type of sensory
information which cause
pleasure, pain or interest are
stored in brain by facilitation of
synaptic pathway.
Example- Spanking.
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11. Cellular basis of Sensitization.
Given by KANDEL
& hiscolleague.
Repeated stimulus.
Ca+2 mediated changes in adenylylcyclase
Increased production of cAMP
neurotransmitter release at synapses.
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12. Due to PresynapticFacilitation
by third interneuron ---
Facilitatory neuron.
which releases SEROTONIN.
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Sensitization
Post synapticneuron
Pre synaptic ending
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13. ASSOCIATIVE LEARNING.
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Classical conditioning.
Learning relationship between
two stimuli.
Pavlovian conditioning.
Operant conditioning.
Learning relationship between
special behavior with a
reinforcement event.
Instrumental or Trial & error
conditioning.
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14. CLASSICAL CONDITIONING.
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Itis a cortical phenomenon.
These are example of higher learning.
Conditioned reflex is Reflex response to a stimuli that previously
elicited little or no response
Acquired by repeatedly pairing given stimulus with another
stimulus which normally produces the response.
Thus temporal association made between neutral conditioned
stimulus (CS)& unconditioned stimulus. (US)
Itdepends upon formation of new functional connections in CNS.
Reinforcement -- CS SHOULD FOLLOWED BY US
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15. CLASSICAL CONDITIONING.
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16. Unconditioned reflex were present in allanimal.
Inborn reflexes
Centre in spinal cord and medulla.
Example- Postural reflexes for maintaining body posture, salivary reflex and sexual
reflexes.
Conditioned reflex are acquired reflex
Certain conditions are required to fulfillit.
Centre- cerebral cortex
Incase of Pavlov experiment the ringing of bell is a neutral stimulus.
Itwill not cause salivation in any dog, unless trained.
For establishment of a conditioned reflex fresh connection are established in the
nervous system between the auditory center and center ofsalivation.

17. Pre-requisites for development of
conditioned reflex.
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Alertness & good health.
Should not be harmful
Reinforcement- once CS is established the pairing of conditioned and unconditioned
stimulus is done at intervals.
Ifyou go on ringing the bell and that’s not followed by giving meat, then nosalivation
occurs. This abolition of reflex is known as InternalInhibition.
Ifthe animal is disturbed by an external stimulus immediately after CS is applied, the CS
may not occurs, Known as External inhibition.
CS should precede on US
Summation- Iffew CS are summated the response is better
.
Discrimination- Animal can discriminate between 2 different stimuli. Eg. Change of
sound frequency of bell cause internalinhibition.
Linking- Animal learns to associate 2 different process.
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18. An immense number of somatic, visceral and other neural changes can bemade
to occur as conditioned reflexresponses.
Conditioning of visceral responses is often called Biofeedback.
The changes include heart rate alteration and BPchanges.
Conditioned decrease in BP has been advocated for treatment ofHTN.

19. OPERANT CONDITIONING.
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Reward conditioning.
Naturally occurring response is
strengthened by positive
reinforcement (reward)
Adversive conditioning.
Naturally occurring response is
Weakened by Negative
reinforcement (Punishment)
Itis to avoid an unpleasant event
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20. Experiment to demonstrate Operant
conditioning.
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21. Experiment to demonstrate Operant
conditioning.
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Positive Reinforcement – pressing a lever is associated with positive
reinforcement, reward i.e. food.
Negative Reinforcement – pressing a lever is associated with Negative
reinforcement, punishment i.e. electric shock.
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22. MEMORY.
Memory –
Acquisition ,
storage &
retrieval of
sensory
information
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23. TYPES OF MEMORY.
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Physiologically on the basis
of how information is
stored & recalled.
Implicit memory.
Explicit memory.
Depending upon
permanency of storage.
Short term.
Intermediate long term.
Long term.
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25. TYPES OF MEMORY.
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Implicit memory.
Non-declarative / reflexive
memory.
How to perform
something.
Not associated with
awareness not involve
processing in
hippocampus.
Explicit memory.
Declarative / Reconition
memory
Factual knowledge of
people, places & things.
Associated with awareness
,Involve processing in
hippocampus.
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26. IMPLICIT MEMORY.
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How to perform something.
Does not depend on conscious
process.
Includes motor skills,
habits,
behavioral reflexes &
learning procedure & rules.
Unconsciousness & automatic
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27. Implicit memory – reflexive learning.
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28. EXPLICIT MEMORY.
Declarative / Recognition
memory
Factual knowledge of
people, places & things.
Associated with
awareness ,Involve
processing in
hippocampus.
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29. EXPLICIT MEMORY.
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About knowledge of
objects, facts and
concepts.
Words & theirmeanings.
SEMANTIC MEMORY EPISODIC MEMORY
Memory of events &
personal experience.
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30. SEMANTIC MEMORY.
Storage of semantic
memory
Indistributed fashion in
different association cortices.
Visual memory
Auditory memory
Somatosensory memory.
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31. TYPES OF MEMORY

32. Damage to cortical area – loss of specific
information
Associative Visual Agnosia –
posterior parietal cortex damage –
can identify but cannot name the
objects.
Appreciative Visual Agnosia –
posterior occipital lobe damage–
can name the objects but cannot
draw
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33. EPISODIC MEMORY.
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Storage of Episodic Memory
Inassociation area of prefrontal cortex.
With other areas of neo-cortex for collection ofinformation
Damage – Amnesia.
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34. MECHANISM OF MEMORY.
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Explicit memory.
Short term memory.
Neural substrate for encoding ofmemory
.
Intermediate long term.
Long term.
Consolidation of memory.
Storage of memory.
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35. MECHANISM OF SHORT TERM MEMORY
Theory of reverberating neurons-
Caused by continual neural activity resulting from nerve signals that travel round and round in
a temporary trace through a circuit of reverberatingneurons.
Presynaptic facilitation or inhibition-
Occurs at synapses that lie on the presynaptic terminals, not on the subsequent
neuron. The neurotransmitter secreted at such terminals frequently cause prolonged
facilitation or inhibition.
Synaptic Potentiation-
Itcan enhance synaptic conduction.
Accumulation of large amount of Ca in presynaptic terminals due to train ofimpulses
passing through.
When amount of Ca become greater than the mitochondria can absorb causes
prolonged presynaptic release of NT
.

36. Working memory.
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37. MECHANISM OF INTERMEDIATELONG
TERM MEMORY
Intermediate Memory
due to temporary physical
or chemical change in pre
or post synaptic
membrane.
Still labile until becomes
long term by process
called – Consolidation.
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38. Mechanism of intermediate Long term memory
Post synaptic neuron
Pre synaptic ending
C
B
A

39. Mechanism of intermediate Long term memory
Mechanism for Habituation-
Results from progressive closure of Ca+2 channel of presynaptic terminalmembrane
Very small entry of Ca+2  very Little amount of NT released.
Mechanism for Facilitation-
Stimulation of facilitator terminal B at the same time of sensory terminalA
Serotonin released by the sensory terminalB
Itacts on the serotonin receptor in sensory terminal Amembrane
Receptor activate enzyme Adenylyl cyclase atmembrane
Formation of cAMP insideA
cAMP activates ProteinKinase

40. Protein kinase cause phosphorylation of a protein that is a part of K+channel at
sensory terminal A
This blocks the channel for K+conductance (mins to Wks)
Lack of K+conductance cause greatly prolonged AP in terminal A (Outflux of K+is
necessary for transmission of AP)
Prolonged AP causes prolonged activation of Ca+2channel
Tremendous quantity of Ca+2 enter into the sensory terminalA
Ca+2 result in increased NT release, thereby greatly facilitating synaptic transmission.

41. LONG TERM MEMORY
The difference is only in degree
Result in actual structural changes (physical restructuring of synapses) ,instead of
chemical changes only
Changes due to DNA which replicate the protein in presynaptic neurons
Also responsible for development of memorytrace.
The changes are-
1. Increase in no. of vescicles release sites for secretion of NT  increase NTrelease by
exocytosis
2. Increase in no. of transmittervescicles
3. Increase in no. of presynaptic terminals
Incontrast to working memory long term memory was improved with exposure ofthe
subject to an enrichedenvironment.
This induce dramatic anatomical changes in cerebral cortex, hippocampusand
cerebellum of brain.
The ability of a neural tissue to change because of its activation is knownas plasticity.

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43. MECHANISM OF LONG TERMMEMORY
Consolidation of Memory
Rehearsal of the sameinformation
again and again in the mind
accelerate and potentiate the
degree of transfer of short term
memory to long termmemory.
For mild – 5-10 min
For strong – 1or more hour
.
Ifthis time not given – retrograde
amnesia
E.g. – Precise time of sleep
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44. PROCESS OF CONSOLIDATION
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Expression of genes
Synthesis of new proteins
Structural changes.
Increase in no of vesicle releasesites
No of vesicles
No of synapticterminals
Change in shape or no of postsynapticspines
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45. CODYFYING THE MEMORIES DURING CONSOLIDATION
Similar information is recalled from the memory storage bin and used to help
process the new information.
Parts involved-
Hippocampus
Thalamus
Prefrontal cortex
Amygdala
neocortex

46. RETRIEVAL OF MEMORY.
Components.
Attentional control system.
Rehearsal system.
Articulatory loop.
Visuospatial sketch pad.
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47. Neural substrate for encoding of memory.
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48. MECHANISM OF LONG TERM
POTENTIATION(LTP)
Itinvolves protein synthesis and growth of presynaptic and postsynaptic neuronsand
their connections.
LTP occurs in many parts of the brain.
Studied on synapses of hippocampus, connection of pyramidal cell in CA 3 and CA1
region via Schaffer Collateral.

49. At the membrane potential, Glutamate release from presynapticnu.
Bind both NMDA and Non-NMDA (AMPA) receptors on postsynaptic nu
Mg+ blocks NMDA receptor so Na+, K+ can flow only through AMPA receptors
Mg+ expel from NMDA due to high frequency tetanic stimulation of presynaptic nu.
Ca+2 influx at postsynaptic neuron
Activation of Ca+2/calmodulin Kinase, Pr
.Kinase C, Tyrosin Kinase (Together induce LTP)
Ca+2/calmodulin complex phosphorylate AMPAreceptors
Increased conductance, more and more of these receptors move to synaptic cell membrane from
cytoplasmic storage site
When LTP induced, chemical signal NO released by postsynaptic nu and pass retrograde to presynaptic
neur
.And produce long term increase in Glutamaterelease

50. MECHANISM OF LONG TERM POTENTIATION
Pre synaptic
ending
Post synaptic
neuron

51. APPLIED ASPECT.
Drugs facilitating learning & memory.
Common CNS stimulant
Caffeine,
amphetamine,
Physostigmine (Inhibit acetylcholinesterase,
prevent breakdown of Ach)
Nicotine (stimulate nicotinic cholinergic
receptors)
Pemoline (stimulate RNAsynthesis)
Mechanism of action.
By facilitating consolidation of energy.
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52. ADDICTION
Morphine
Amphetamine
Cocaine
Heroin
Nicotine
Alcohol
All these produces Dopamine on the limbic system on nu.Accumbens
All stimulate reward area.

53. AMNESIA.
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Antegrade.
Inability to establish new long term
memories
Mostly in lesions involving
hippocampus.
Retrograde –
Inability to recall past memories.
Amnesia greater for recent pastthan
remote past.
Lesions involving temporal lobe
(Temporal lobe syndrome)
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54. SENILE DEMENTIA.
Syndrome in elderly people
characterized by progressive
impairment of memory &
cognitive capacity.
Causes –
Alzheimer’sdisease,
Cerebrovascular disease,
Parkinsonism,
Lewy body dementia,
Prion disease
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55. Alzheimer’sdisease.
Senile dementia
Prototypical neurodegenerative disease.
Degeneration of pathways from septal region
of the forebrain to thehippocampus.
Affecting 15-25%people over 65
Cholinergic neurons cease functions.
Associated with decrease release of Ach in
some area of brain.
Loss of postsynaptic neurons.
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56. CHARACTERISTIC FEATURES.
Loss of recent memory.
Impairment in other areas of
cognition –
language,
problem solving,
judgment,
calculation,
attention.
Psychiatric symptoms
Loss of spatial orientation.
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57. CONCEPT OF DOMINANT HEMISPHERE.
Interpretive
functions of
Wernicke’s area,
Angular gyrus &
Frontal motor
speech area –more
developed in
Dominant
hemisphere.
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58. CONCEPT OF DOMINANT HEMISPHERE
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95%left hemisphere is dominant.
Wernicke’s area in Non-dominant
is concerned with
emotional content,
intonation of spoken language,
understanding & interpreting
non-verbal, visual & auditory
experiences as interpretation of
Music.
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59. CONCEPT OF CATEGORICAL &
REPRESENTATIONAL HEMISPHERE.
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Functions allotted to left
hemisphere in right handed person.
Right hand control.
Spoken language.
Written language.
Mathematical skills.
Scientific skills.
Reasoning.
Functions allotted to right
hemisphere in right handed person.
Left hand control.
Music awareness.
Three dimensional awareness.
Art awareness.
Insight.
Imagination.
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Thank You
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