This document discusses physiology of memory and learning. It defines learning as a relatively permanent change in behavior due to experience, while memory is the ability to recall past events. There are two main types of learning - associative and non-associative. Associative learning involves associating stimuli, like in classical and operant conditioning. Non-associative learning does not require association of stimuli, and includes habituation and sensitization. Memory is classified into sensory, short-term, long-term and permanent memory based on duration. The hippocampus and surrounding areas are involved in consolidating memories by converting them from short-term to long-term storage through long-term potentiation.

1. Physiology of Memory
and Learning

2. Memory an Learning
• Learning and memory are higher-level
functions of the nervous system.
• Learning is change in the behavior on the
basis of past experiences.
• Memory is the ability to recall the past
events or facts.

3. Learning
• ♦ Def
• It is the acquisition of knowledge or skills as
a result of experiences and consequently it
can alter behavior on basis of experiences
• Learning refers to a more or less permanent
change in behavior which occurs as a result of
practice (Kimble, 1961)

4. Learning
• Types
1. Associative
(Relation of one
stimulus to another)
a. Classic
conditioning
b. Operant
conditioning
2. Non-associative
(ignore or react )
a.
Habituation
b.
Sensitization

5. Associative Learning
• In this type of learning, the subject learns
about the relationship that can associate one
stimulus to another
• It is a conditioned process which results in
the formation of learned responses called
conditioned reflexes
• Conditioned reflex is an automatic response
to a stimulus (conditioned stimulus) which did
not previously evoke response acquired by
repeatedly associating this stimulus with
another stimulus (unconditioned stimulus)
•

6. a) Classic Conditioning
• This type of conditioned reflexes was 1st
described by Pavlov (Russian Physiologist)
• He noticed that his experimental dogs salivate
just on seeing the animal house keeper who used
to feed
• Some sort of association had developed in the
brains of these animals between visual stimuli
related to seeing the housekeeper (conditioned
stimulus) and food ingestion (unconditioned
stimulus for salivation when food is placed in
mouth)

7. a) Classic Conditioning

8. a) Classic Conditioning
• This type of conditioning can be integrated a
different levels of CNS
• Requirements:
• 1) CS applied before US
• 2) Pairing must occur several times
• 3) No separation between the CS and US

9. a) Classic Conditioning

10. b) Operant Conditioning
• In this type of conditioning the subject is taught
to perform some voluntary action in response to a
particular stimulus (visual or sound stimulus) that
alert him to perform the learned action in order
to obtain reward to avoid punishment
• Alerting signal acts as conditioned stimulus
whereas pleasant or unpleasant event that follow
performance of learned response represents
unconditioned stimulus

11. b) Operant Conditioning

12. b) Operant Conditioning
Example:
• Car driver and traffic light
• The car driver stops the car on seeing the red
traffic light and drives on seeing the green light
Integration:
• Hippocampus and amygdala are important in
linking the stimulus to the operation
• Integration occurs in CC especially orbitofrontal
cortex

13. Non-associative Learning
• In this type of learning, the subject learns
whether to ignore or react to a certain
stimulus
• It is a simple way of learning that does not
need association between 2 stimuli
• It is 2 types;
• A) Habituation
• B) Sensitization

14. Habituation
• It is a gradual decrease in the response to
stimulus when it is frequently repeated
• It is simple and widespread
• Examples:
• A loud and unexpected sound produces looking
towards the source of sound, change in heart
rate, and change in blood pressure
• If the sound turns to be insignificant, its
repetition results in little or no response

15. Habituation
• It is a stimulus specific e.g. traffic noise and
mother and baby
• Mechanism:
• Repetition of the stimulus close Ca channels in
presynaptic neurons →↓ Ca influx →↓ release of
neurotransmitters →↓ behavioral responses to the
stimulus

16. Habituation
• Experiments performed in Aplysia californica

17. Sensitization
• It is a potentiation in the response to stimulus
(painful or pleasant) when it is frequently
repeated
• It is simple and widespread
• Examples:
• One normally ignore stray dogs by habituation, but
if he is bitten, he will become more attentive and
develop aversion reaction to them for long time
• Stimulus specific:
• One who is bitten by dogs will not be afraid of
donkeys or cows

18. Sensitization
• Mechanism:
• Strong or noxious stimulus → facilitating
interneurons (serotonin) →↑ cAMP in presynaptic
neurons → block of K channels → depolarization
of presynaptic neurons → keep Ca channels open
→↑ Ca influx →↑ release of neurotransmitters
→↑ behavioral response to mild stimuli

19. Sensitization

20. Sensitization

21. Memory
• Def
• It is the ability of the brain to store information
and recall it at later time
• Capacity of the brain:
• It is limited (total capacity of brain is 3x 108
bits)
• So, informations entering brain are either;
A. Selected and stored (1%) → most important
B. Other (99%) → are neglected and forgotten

22. Memory• Information Unit:
• It is bit
• A bit is the simplest form of sensory experience i.e.
figure, sound, touch , or smell
• All sensory systems send information to brain at 50
bit/sec
• E.g. during reading 40 bits/sec, during mental
calculation 12 bits/ sec, and during counting 3 bits
/sec
• Average rate of flow of information is 20 bits/sec
• For learning a language about 40- 50 millions bits
should be stored in memory
• To store 1 bit, 10 neurons are required

23. MemoryClassification of memory:

25. 1. Sensory Memory
• Duration: very short (about 0.5 seconds)
• Capacity: very small (15-20 bits)
• Entry into storage: automatic during perception
• Access to storage: very rapid
1. Vision: iconic memory
2. Hearing: echoic memory
• Mechanism:
• 1. Stimulation of reverberating circuits →
repeated activation of neurons
• 2. Synaptic sensitization if sensory experience
coupled with painful stimuli

26. 1. Sensory Memory
• Mechanism:
• 3. Posttetanic potentiation: multiple stimuli
at presynaptic terminal →↑ Ca content in
presynaptic terminal →↑ release of
neurotransmitters
• Mechanism of forgetting:
• 1. Fading (spontaneous and gradual decline in the
amount of information)
• 2. Extinction (spont. disappearance of
information from memory)

27. 2. Short-term Memory
• Duration: (min to hours)
• Entry into storage: verbalization (describing the items in words)
• Recall or access to storage: rapid
• Mechanism:
• Made by formation of temporary memory traces

28. 2. Short-term Memory
• Memory trace:
• Is a newly developed pathway or signal transmission
resulting from facilitation of new synapses → creation of
new circuits in the brain
• This occurs by
• 1. Long term potentiation of synapses
• 2. Changes in physical properties of postsynaptic
membrane → ↑ sensitivity to chemical transmitters
• Mechanism of forgetting:
• New information replaces old

29. 3. Long-term Memory
• Duration: (hours to years )
• Capacity
• Very large
• Information stored according to its significance
• Entry into storage: practice or and punishment or reward
• Recall or access to storage: slow
• Mechanism:
• Made by formation of memory engrams (long-lasting memory
traces) formed by structural changes in presynaptic terminals

30. Long-term potentiation
• 1. The binding of glutamate to its NMDA receptors and
simultaneous depolarization of the postsynaptic
membrane causes the NMDA receptor channels to open.
• 2. This opening of the NMDA receptor channels allows
Ca2+ to enter.
• 3. The entry of Ca2+ into the postsynaptic neuron causes
long-term potentiation in that neuron.
• 4. The entry of Ca2+ into the postsynaptic neuron also
activates nitric oxide synthase, causing nitric oxide
production.
• 5. The nitric oxide then acts as a retrograde messenger,
diffusing into the presynaptic neuron and somehow
causing it to release more neurotransmitter.

32. 3. Long-term Memory
• Mechanism:
• memory engrams made up by;
• 1. increase in number of vesicles
• 2. increase in number of presynaptic terminals
• 3. increase in release sites of chemical transmitters
• 4. generation of new receptor sites
• 5. long term potentiation
• Engrams remain for long time up to several years
• Formation of new engrams requires protein synthesis

33. 3. Long-term Memory
• Mechanism of forgetting:
1. Proactive inhibition by previously stored materials
(more common)
2. Retroactive inhibition by subsequently stored
material

34. 4. Permanent Memory
• Duration: (permanent)
• Capacity
• Very large
• Entry into storage: very frequent practice
• Recall or access to storage: very rapid (recall not affected by brain
injury (like name, write, and read)
• Mechanism:
• Advanced stage of long-term(permanent engrams)
• Mechanism of forgetting :
• No forgetting

35. Phases of memory
• Encoding-information for each memory is assembled from
the different sensory systems and translated into whatever
form necessary to be remembered.This is presumably the
domain of the association cortices and perhaps other areas.
• Consolidation-converting the encoded information into a
form that can be permanently stored.The hippocampal and
surrounding areas apparently accomplish this.
• Storage-the actual deposition of the memories into the final
resting places–this is though to be in association cortex.
• Retrieval-memories are of little use if they cannot be read out
for later use. Less is known about this process.
•

36. Encoding of memory
• It means classification and placing memory items in their
proper memory stores in brain
• Brain areas concerned with encoding of long term memory;
• 1. Hippocampus (major central role) all bits of information go
to it first
• 2. Amygdala (emotional memory)
• 3. Basal forebrain (Nucleus basalis or Meynerts nucleus)
• 4. Noecortex
• 5. Mammillary body of hypothalamus
• 6. Orbitofrontal cortex

37. Consolidation of memory
• It means the process of conversion
of STM to LTM
• It takes from 5 min to 2 hrs
• It is interrupted by
1. Deep anaesthesia
2. Brain concussion
3. Electroconvulsive therapy

38. Brain Regions involved in Consolidation of
memory
• Hippocampus
• Anterior & lateral
temporal lobe,
• Medial temporal lobe
• Amygdala

39. Hippocampus and Consolidation of memory
• The hippocampal region is critical for the consolidation of
information in long-term memory
Evidence
Three major excitatory neural components of the hippocampus
Perforant pathway
• forms excitatory connections between the parahippocampal cortex
and the granule cells of the dentate gyrus
Mossy fibers
• connect the granule cells of the dentate gyrus to the pyramidal cells
Schaffer collaterals
• connect the CA3 pyramidal cells to the CA1 pyramidal cells

40. Disorders of Memory
1) Amnesia → loss or impairment of memory
•It may be;
a) Retrograde amnesia
•It means inability to recall memories from the past
(retrograde: going backwards), that is from the long-
term memory stores.
•Transient brain malfunction erase 1ry memory
•It usually follows a traumatic event that interferes with
the normal activity of the brain, such as a strong brain
concussion and vascular strokes

41. Disorders of Memory
• b)Anterograde amnesia
• It is the inability to store new information in the
long-term memory for later recall.
• It usually results from lesions of the medial portions
of the temporal lobe, a region that include the
hippocampus, amygdala, and the adjacent areas of the
temporal
• c) psychogenic or hysterical amnesia
• Rare
• Sudden loss of memory of all information
• Exposure to severe psychological stress

42. Disorders of Memory
2) Senile dementia and Alzheimer disease
It occurs in old age (senile dementia) and middle age
(Alzheimer), but it can occur at any age
• It is characterized by impairment of memory, lack of
concentration, inattentiveness
• Incidence: 10-15 % after age of 65 years
• Mechanism:
• Loss of cholinergic terminals that diffuse from
nucleus basalis to neocortex, amygdala and
hippocampus