The document discusses learning and memory. It explains that learning involves how experience changes the brain, while memory involves how these changes are stored and retrieved. It describes the different types of memory (sensory, short-term, long-term) and where memories are stored in the brain. The case of patient H.M., who had medial temporal lobe removal, demonstrated the role of these areas in forming new memories and provided evidence for separate short-term and long-term memory systems. Concussions can cause retrograde and anterograde amnesia, providing evidence that memories are consolidated over time.

1. Learning and Memory

2. The brain changes its
functioning in response
to experience
 Learning
 relatively permanent change in behavior as a
function of training, practice or experience
 how experience changes the brain
 The process by which we acquire knowledge about
the world
 “more or less a permanent change in behavior
which occurs as a result of practice

3. The Stages of Learning
 Acquiring wherein one masters a new
activity…
 Retaining the new acquisition for a period of
time
 Remembering which enables one to
reproduce the learned act or memorized
material.

4. MEMORY IS A PHASE OF
LEARNING

5.  Memory
 How changes are stored and
subsequently reactive
 The process by which that
knowledge of the world is encoded,
stored, and later retrieved

6. Three Major Categories of
Memory
 Awareness of briefly presented information
and perception of its aftereffects refers to
sensory memory
 Two forms:
Echoic Memory auditory stimuli stored
for a few seconds that is necessary for
comprehending sounds.
Iconic Memory the visual representation
of information in the environment

7.  Short term Memory retains small amounts
of information for a few seconds or less than
30 seconds.
 Long Term Memory is a mental storage
where we keep our knowledge and
experiences for a relatively permanent period
of time.

8. Categories of LTM
Declarative Memory
 Holds information that are easily verbalized and
described such names of people, concepts, events and
experiences.
Sub types:
Semantic memory
Episodic Memory
Procedural Memory
 holds relatively permanent information that are not
easily verbalized.

9.  Explicit Memory
 knowledge of facts- people, places and the
things-meaning of these facts.
 Conscious memory
 Implicit Memory
 Involves information on how to perform
something; it is recalled unconsciously
 Used in trained, reflexive motor or perceptual
skills.

10. Where are Memories Stored?
 Memory Storage
 Stored diffusely throughout the
structures of the brain.
 Five areas of the brain have been
implicated in the storage of man’s
memory.
 They are Inferotemporal Cortex,
Amygdala, Prefrontal Cortex,
Cerebellum and Striatum

11. INFEROTEMPORAL CORTEX
 Is the cortex of the inferior
temporal lobe. It is involved in the
visual perception of objects. It is
thought to participate in storing
memories of visual patterns.

12. Amygdala
 An almond shaped nucleus in the
anterior temporal lobe. It play a role
in memory for emotional significance
of experiences.

13. Prefrontal Cortex
 It is composed of numerous anatomically
distinct areas that have different connections
and functions. There are regions of prefrontal
cortex that perform fundamental cognitive
processes during all working memory tasks.
Involved in the memory for the temporal
order of events.

14. Cerebellum
 Is thought to store memories of
learned sensorimotor skills.

15. Striatum
 it stores memories for consistent
relationships between stimuli and responses-
the type of memories that develop
incrementally over man trials.

16. The Hippocampus and Memory for
Spatial Location

17. The Hippocampus

18.  It forms part of the limbic system
which is composed of brain structures
that play a role in memory, emotion
and motivation.
 The hippocampus and surrounding
structures are thought to play crucial
roles in the encoding and retrieval of
memories

19. Spatial Orientation
 Three types of Spatial Ability
 Ability to visualize rotation and flipping
over of shapes and diagrams
 Ability to reorient objects from different
angles
 Finding relations between different
spatial objects.

20. The Hippocampus and Spatial
Orientation
 The hippocampus helps construct
a 3D “mental map” of our
surroundings, and is crucial for our
ability to move around in the real
world.

21. What is:
Lobectomy – removal of a lobe or
major part of one from the brain.
Lobotomy – Separation of a lobe or a
major part of one from the rest of the
brain by a large cut but is not
removed

22.  Bilateral Medial Temporal Lobectomy
the removal of the medial portions
of both temporal lobes, including
most of the hippocampus, amygdala
and adjacent cortex.

24. Amnesic Effects of Bilateral
MedialTemporal
Lobectomy

25. AMNESIA
is a deficit in memory
caused by brain
damage, disease, or
psychological trauma.

26. There are two main types of
amnesia:
retrograde amnesia
and anterograde
amnesia.

27. Retrograde amnesia is the
inability to retrieve
information that was acquired
before a particular date,
usually the date of an accident
or operation.

28. Anterograde amnesia is the
inability to transfer new
information from the
short-term store into the
long-term store.

29. The Brain’s ability to
change its
functioning in
response to
experience.

30.  Learning deals with how
experience changes the brain.
 Memory deals with how these
changes are stored and
subsequently reactivated.

31. What is:
 Lobectomy:is an operation in
which a lobe, or a major part of
one, is removed from the brain.
 Lobotomy: Separation of a lobe
or a major part of one from the
rest of the brain by large cut but
is not removed.

32. What is:
 Bilateral Medial Temporal Lobectomy
The removal of the medial
portions of both temporal
lobes, including most of the
hippocampus, and amygdala.

35. Effects of Bilateral Medial
Temporal Lobectomy
The Case of H. M., The Man Who Changed
the Study of Memory
Henry Molaison also known as H.M. – an
epileptic who had his temporal lobes
removed in 1953.

37. His seizures were
dramatically reduces- but so
was his memory
Mild retrograde amnesia and
severe anterograde amnesia

38. Formal Assessment of H.M.
 Digit Span – H.M. can repeat
digits provided the time between
learning and recall is within the
duration of STM.

39. Formal Assessment of H.M.
 Block-tapping memory –span test
– this test demonstrated that
H.M. has global amnesia–
amnesia for information
presented in all sensory modality

40. Formal Assessment of H.M.
 H.M. readily “learns” responses through
classical conditioning, but has no
memory of conditioning trials

41. Scientific Contributions of
H.M.’s Case
 Medial temporal lobes are
involved in memory
 STM and LTM are distinctly
separate – H.M. is unable to
move memories from STM to
LTM, a problem with memory
consolidation

42. Medial Temporal Lobe Amnesia
 Semantic Memory (General
information) may function
normally while episodic memory
(events that one has experienced)
does not- they are able to learn
facts, but do not remember doing
so.

43. Medial Temporal Lobe Amnesia
Not all with this form of
amnesia are unable to form
new explicit long-term
memories

44. Amnesia after Concussion :Amnesia after Concussion :
Evidence for ConsolidationEvidence for Consolidation
Amnesia of Korsakoff’sAmnesia of Korsakoff’s
SyndromeSyndrome

45. What is:
Concussion
- a temporary disturbance of consciousness
produced by a nonpenetrating head injury
Posttraumatic Amnesia
-an amnesia following a nonpenetrating blow
in the head

46. Amnesia after
Concussion: Evidence for
Consolidation Concussions may cause retrograde amnesia for
the period before the blow and some anterograde
amnesia after
 The same is seen with comas, with the severity of
the amnesia correlated with the duration of the
coma
 Period of anterograde amnesia suggests a
temporary failure of memory consolidation

47. Gradients of Retrograde Amnesia and
Memory Consolidation
 Concussions disrupt consolidation (storage) of recent
memories
 Hebb’s theory – memories are stored in the short term
by neural activity
 Interference with this activity prevents memory
consolidation. Examples:
 Blows to the head (i.e., concussion)
 ECS (electronconvulsive shock)
 Long gradients of retrograde amnesia are inconsistent
with consolidation theory

48. Reconsolidation
 Each time a memory is retrieved
from LTM, it is temporarily held in
STM
 Memory in STM is susceptible to
post-traumatic amnesia until it is
reconsolidated

49. The Hippocampus and
Consolidation
 H.M. has some retrograde amnesia
 Perhaps the hippocampus stores memories
temporarily (standard consolidation theory)
 Consistent with the temporally graded
retrograde amnesia seen in experimental
animals with temporal lobe lesions
 Or, perhaps the hippocampus stores memories
permanently, but they become “stronger” over
time

50. What is:
Korsakoff’s (Korsakov’s) Syndrome
- a brain disorder caused by the lack of
thiamine (vit.B1) in the brain
- it was named after the
neuropsychiatrist Sergei Korsakoff
who popularized the theory

51. Six Major Symptoms:
1. Anterograde Amnesia
2. Retrograde Amnesia
3. Confabulation- invented memories
which are taken as true due to gaps
in memory
4. Meager content in conversation
5. Lack of insight

52. Amnesia of Korsakoff’s
Syndrome
 Most commonly seen in alcoholics
(or others with a thiamine
deficiency)
 Amnesia, confusion, personality
changes, and physical problems
 Typically damage in the pre frontal
cortex – medial thalamus + medial
hypothalamus

53. Amnesia of Korsakoff’s
Syndrome (continued)
 Amnesia comparable to medial temporal
lobe amnesia in the early stages
 Anterograde amnesia for episodic
memories
 Differs in later stages
 Severe retrograde amnesia develops
 Differs in that it is progressive,
complicating its study

55. • Alzheimer’s disease is associated
with a gradually progressive loss of
memory often occurring in old age.
• Affects 50% of people over 85.
• Early onset seems to be influenced
by genes, but 99% of cases are late
onset.
• About half of all patients with late
onset have no known relative with
the disease.

56. • Alzheimer’s disease is associated with
an accumulation and clumping of the
following brain proteins:
Amyloid beta protein 42 which produces
widespread atrophy of the cerebral cortex,
hippocampus and other areas.
An abnormal form of the tau protein, part
of the intracellular support system of
neurons.

57.  Accumulation of the tau protein results
in:
 Plaques – structures formed from
degenerating neurons.
 Tangles – structures formed from
degenerating structures within a
neuronal body.

59.  A major area of damage is the basal forebrain and
treatment includes enhancing acetylcholine
activity.
 One experimental treatment includes the
stimulation of cannabinoid receptors that limits
overstimulation by glutamate.
 Research with mice suggests the possibility of
immunizing against Alzheimer’s by stimulating the
production of antibodies against amyloid beta
protein.