memory

1. MEMORY

2.  Introduction
 Processes involved in memory function
 Theories of memory
 Classification of memory
 How knowledge represented and organized in
memory
 Retrieval
 Forgetting- when memory lapses and why we
forget
 Neuroanatomical correlates- History,leison study,
imaging study
 Neurochemical correlates
 Neuropsychological assessment test of memory
 Conclusion

3.  Without memory, life would perpetually be spent
in ‘here and now’.
 Memory provides the essential substrate for
cognitive activities that define experience;
development of personality and the possibility of
growth and change.
 Memory is an integral part of our existence, yet it
is only vaguely understood.
 Memory is the power or process of reproducing or
recalling what has been learned and retained
especially through associate mechanisms
(Webster‟s dictionary, 1967).

4.  Memory is fundamental to all learning and
development,including personality and
interpersonal relationships (Singer 1995 ).
 Just as memory functions largely outside of
conscious awareness (Rugg 1995 ), we are
often less than fully conscious of the extent to
which even mild memory deficits can
interfere with one’s
 social and occupational functioning (Squire
1982 ),
 and the extent to which nearly all
psychotherapies rely on intact learning and
memory.

5.  3 distinct process of memory are:
 Encoding
 Storage
 Retrieval

7.  Automatic Processing - unconscious encoding of
incidental information, such as space, time, frequency,
and well-learned information, such as word meanings.
 Effortful Processing - encoding that requires
attention and conscious effort. What you learn in the book
and in this class!
 After practice, some effortful processing becomes
automatic
Encoding
Effortful Automatic

8.  Encoding Meaning - including meaning of
words
 Acoustic Encoding - encoding of sound
especially sound of words
 Visual Encoding - encoding of picture
images.
 Encoding may be faulty due to emotion
and distress experienced at the time of
incident.

9.  Information Processing Theory: (Atkinson-
Shiffrin 1968)

10.  Shortest duration time, only 0.5 to 2.0
seconds
 2 types - iconic and echoic memory.
 According to the Atkinson and Shiffrin model
of memory, only iconic memory is equal to
sensory memory.
 The addition of echoic memory to the level
of sensory memory is due to research done
by Darwin and others (1972).

11.  STM holds information received from sensory
register for upto 30 secs although the length
of the retention depends on a number of
factors.
 Recall depends on where an item is in a series
of items – Serial position effect(Glanzer &
Cunitz,1966)
 Primacy effect
 Recency effect
 has a capacity for 7+/- 2 items. George Miller’s
“magical” number
 -

13. 0
10
20
30
40
50
60
70
80
90
3 6 9 12 15 18
Time in seconds between presentation
of contestants and recall request
(no rehearsal allowed)
Percentage
who recalled
consonants
Rapid decay
with no
rehearsal

14.  Chunking - a useful method to memorize
more than just single items.
 Gobet et al. defined a chunk as "a collection
of elements that are strongly associated with
one another but are weakly associated with
other chunks“
 Most commonly we use it in memorizing
telephone numbers e.g. 9-4-3-2-8-9-1-9-3-2
would be chunked into 9432-891-932
 Fate of information in STM
 Displaced by incoming items and lost
 Before lost some of the information retrieved
and used
 Passed along the next memory stage -LTM

15.  Consists of keeping items of information in
the centre of attention, perhaps by repeating
them silently or aloud.
 Elaborative rehearsal
 Maintainance rehearsal
 Formar one is more likely to organize the
information in STM to LTM.

16.  Approx duration- days, months, years or a
lifetime
 Capacity- very large no known limit
 Types of information stored- primrily
meaningful sentences,life events and
concepts,some images; semantic and
episodic memory.

17.  Strengths
 Many memory studies provide evidence to
support the distinction between STM and LTM
(in terms of encoding, duration and
capacity).
 The model can account for primacy &
recency effect.
 The model is influential as it has generated a
lot of research into memory.

18.  Model is oversimplified
 Cases have been reported where patients can form
long term memories even though their STM-abilities
are severely reduced.
 Shallice and Warrington (1970) suggested- there
must be another possible way for information to
enter LTM than via STM.
 Baddeley and Hitch (1974)-Under certain condition
it seems to be possible to do two different tasks
simultaneously.
 The model suggests-rehearsal helps to transfer
information into LTM but this is not essential.
 Emphasis on structure and neglect the process
elements of memory (e.g. it only focuses on
attention and rehearsal).
 a passive/one way/linear model.

19.  Craik and Lockhart (1972): incoming
information is processed at different levels
 Levels of processing:
 Structural = shallow (structure of stimulus)
 Phonemic = intermediate (what word sounds
like)
 Semantic = deep (meaning of verbal input;
thinking about the objects and actions the
words represent)
 Deeper processing = longer lasting memory
codes

21. Strengths
 The theory is an improvement on Atkinson &
Shiffrin’s account of transfer from STM to LTM.
 Showed that encoding not a simple,
straightforward process.
 Widened the focus from seeing long-term
memory as a simple storage unit to seeing it as a
complex processing system.
 Explains why we remember some things much
better and for much longer than others.
 This explanation of memory is useful in everyday
life because it highlights the way in which
elaboration, which requires deeper processing of
information, can aid memory.

22.  Weaknesses
 Despite these strengths, there are a number of
criticisms of the levels of processing theory:
 It does not explain how the deeper processing
results in better memories.
 Deeper processing takes more effort than
shallow processing and it could be this, rather
than the depth of processing that makes it more
likely people will remember something.
 The concept of depth is vague and cannot be
observed. Therefore, it cannot be objectively
measured.

23.  "Working memory is a limited capacity system
for temporary storage and manipulation of
information for complex tasks such as
comprehension, learning and reasoning" –
Baddley
 4 components of working memory
 Phonological rehearsal loop
 Visuospatial sketchpad
 Executive control system
 Episodic buffer

25.  by duration - sensory memory, short term
memory, and long term memory.
 by temporal direction- retrospective memory
(the content to be remembered is in the past) and
Prospective memory (the content is to be
remembered in the future)
 by information type (long-term memory) –
Declarative and non- Declarative
 Explicit-implicit taxonomy by Tulving, Schacter
and Stark, 1982.
 Declarative-procedural distinction by Cohen and
Squire, 1980.

26.  Available to conscious retrieval
 Can be declared (propositional)
 Flexible
 Types-Episodic and Semantic
 Episodic- Memory for personally experienced
events that occurred in particular place at a
specific time (defined by Tulving, 1972)
 Contextual, spatiotemporal, autobiographical,
“remembering”
 Example -“What did I eat for breakfast?”
 Semantic - Memory for facts, general
knowledge, word meanings
 Acontextual: Independent of where or
when the information was encoded
 Example- “What is the capital of India?”

27.  Experience-based change in behaviour
 Cannot be declared(Procedural)
 Slow,reliable and inflexible
 There is no conscious access
Types

Procedural Priming Conditioning Non-associative learning
-sensorimotor –conceptual –classic -habituation
-cognitive -perceptual –instrumental –sensitization
-perceptual

28.  Skills and habits: Skills are procedures
(motor, perceptual or cognitive) that are
attained for operating in the world.
 Habits are dispositions and tendencies
specific to a set of stimuli and that guide
behavior.
 Requires multiple trials
 Example-riding a bi-cycle
 Priming: refers to facilitation of the ability
to detect or identify particular stimuli
based on specific recent experiences with
them.

29.  Conditioning: Conditioned stimulus
followed by an unconditioned stimulus
leads to an unconditioned response and
later this response follows the conditioned
stimulus.
 Non-associative learning: these refer to
changes in already existing responses to
stimuli, as in reflex responses, fixed action
patterns.
 It involves:
 Habituation: decrease in response to
repeated stimuli.
 Sensitization: increase in response to
strong stimuli.

30.  What forms do our mental representations
of information take?
 Clustering—tendency to remember similar or
related items in groups
 Conceptual hierarchy—multilevel classification
system based on common properties among items
 Schemas—organized cluster of knowledge about a
particular object or event abstracted from
previous experience w/the object or event
(professor’s office example)

31.  What forms do our mental representations
of information take?
 Semantic Networks—consists of nodes
representing concepts, joined together by
pathways that link related concepts
 Explain why thinking about one word (butter)
can make a closely related word (bread)
easier to remember; thinking about a word,
thoughts naturally go to related words

33.  The tip-of-the-tongue phenomenon- involves a
temporary inability to remember something
you know and a feeling that the memory is
just out of reach.
 The TOT phenomenon shows that recall can
often be jogged by retrieval cues – stimuli
that help gain access to memories.
 Recalling an event
 Context cues—helps to put yourself back into
context in which event occurred
 Reconstructing memories
 Misinformation effect
 Source monitoring
 Reality monotoring

35. 0
10
20
30
40
Water/
land
Land/
water
Water/
water
Different contexts for
hearing and recall
Same contexts
for hearing and
recall
Land/
land
Percentage of
words recalled

36.  Ebbinghaus and Memory
 Pioneering researcher in
field of memory
-established method to quantify
memory performance and
describe basic findings.
-Used nonsense syllables
- The amount remembered
depends on the time spent learning
H. Ebbinghaus (1850-1909)

37. Most forgetting occurs
right after learning
-approx. 50% in first 40
min
Relationship between
delay and forgetting NOT
linear
Other important findings Beneficial effects of
distributed practice for repetitions (ie., ‘spacing
effect’)
-List-length effect

38.  Mood-Congruent Memory
 tendency to recall experiences that
are consistent with one’s current
mood.
 Depression and alcohol are excellent
examples of the phenomenon of mood-
congruent memory.
 Depression disrupts encoding and
alcohol disrupts storage.
 What people learn when depressed or
drunk won’t be recalled well in ANY
state.
 However, they will be more likely to
recall this info when depressed or
drunk.

39.  Measures of Forgetting
 Recall- involves requiring subjects to
reproduce information on their own
without any cues
 Recognition- involves requiring subjects
to select previously learned material from
an array of options
 (multiple-choice vs. essay exams).

40.  Ineffective Encoding—may never have been
inserted into memory in the first place
(pseudoforgetting)
 Decay theory—claims memory traces fade
w/time
 Interference theory
 Proactive—previously learned info interferes
 Retroactive—new info impairs retention of
previously learned info
 Encoding specificity principle—value of a
retrieval code depends on how well it
corresponds to the memory code (phonemic,
semantic)

41. Effects of interference. According to interference theory, more
interference from competing information should produce more
forgetting. McGeoch and McDonald (1931) controlled the amount of
interference with a learning task by varying the similarity of an
intervening task. The results were consistent with interference theory.
The amount of interference is greatest at the left of the graph, as is the
amount of forgetting. As interference decreases (moving to the right on
the graph), retention improves. (Data from McGeoch & McDonald, 1931)

42. Retroactive and proactive interference. Retroactive interference
occurs when learning produces a “backward” effect, reducing recall of
previously learned material. Proactive interference occurs when learning
produces a “forward” effect, reducing recall of subsequently learned
material. For example, if you were to prepare for an economics test and
then study psychology, the interference from the psychology study would
be retroactive interference. However, if you studied psychology first and
then economics, the interference from the psychology study would be
proactive interference

43.  While the concept of repression has been around
for a century, interest in this phenomenon has
recently surged due to many prominent reports of
repressed memories of child sexual abuse.
 The authenticity of these repressed memories is
challenged by empirical studies that show that it is
not at all hard to create false memories and that
many recovered memories are actually the
product of suggestion.
 Roediger and McDermott (2000) have shown that
when participants are asked to learn a list of
words, and another target word that is not on the
list but is strongly associated with the learned
words is presented, the subjects remember the
non-presented target word over 50% of the time.
On a recognition test, they remember it about
80% of the time–a memory illusion.

44.  While research clearly shows that memories
can be created by suggestion, in cases of
child sexual abuse memories, for example,
this issue becomes quite emotionally charged.
 Some cases of recovered memories are
authentic, and we don’t yet have adequate
data to estimate what proportion of recovered
memories of abuse are authentic and what
proportion are not.
 Still, this controversy has helped inspire a
great deal of research that has increased our
understanding of just how fragile, fallible,
malleable, and subjective human memory is.

45.  Whereas the previous models have aided in
understanding memory, the question of the
anatomical correlates of these stores remains.
 Efforts have been bounded by the
level of technology available.
 Earlier efforts involved:
 Phrenology-Gall and Spursheim
in mid 1800’s used the countenances
of the skull as correlating to the
cortex underneath and on basis of
the bumps would predict the strong
and weak faculties present in an
individual.

46.  In the beginning of the 20th century,
Karl Lashley on the basis of his
experiments propounded
 Theory of mass action: entire
cortex involved in all functions .
 Theory of equipotentiality: each
cortical region can assume control of any
given behavior.
 However, both were subsequently debunked.
 Presently, the techniques used are
 1.Tissue examination
 2.Lesion studies
 3.In-vivo imaging

47.  1.Tissue examination is involved in the cellular
processes involved in memory.
 2.Regional Lesion analysis-
 Generic study of brain injury and its effects on
memory. (Gabrieli 1995).
 Major types of “regional amnesia” based on injury or
lesion of a particular brain region.
 A)Diencephalon type: e.g Korsakoff’s
syndrome (KS)
 Findings:
 Normal STM
 Profound impairment in declarative LTM.
 Pronounced anterograde amnesia.
 Retrograde amnesia less profound.
o Diencephalon lesions also show temporal order
memory dysfunction. (Parkin et al 1990)

48. Retrograde versus anterograde amnesia. In retrograde amnesia,
memory for events that occurred prior to the onset of amnesia is
lost. In anterograde amnesia, memory for events that occur
subsequent to the onset of amnesia suffers.

49.  2.Temporal lobe type: e.g. Herpes encephalitis
 Mostly medial temporal lobe damage that
includes:
 Hippocampi, amygdalae, perirhinal,
enterorhinal, parahippocampal areas.
 Symptoms in such cases is mostly similar to the
patients with KS but with better insight, more
involvement of the retrograde memories.
 In addition:
 Right hippocampus lesions: spatial memory
dysfunction. (Kopelman 1997)
 Left inferolateral temporal lobe: semantic
memory dysfunction
 Right temporal lobe damage: impairment in face
recognition memory (Eisenger et al 1996)

51.  Temporal lobe lesions: spatial memory is
maximally affected. (Hunkin et al 1994)
 Similar cases of TL damage have been studies
extensively (Milner 1965, Zola- Morgan et al
1986) and conclusions in addition to above
have been:
 TL is not involved in STM
 Hippocampus is important in formation of
new explicit declarative LTM (Consolidation)
 LTM is not stored in hippocampus
 To sum up, explicit/declarative memory loss,
episodic memory loss, and anterograde memory
loss more than retrograde memory loss; implicit
memory is not affected.

52.  The dorso-lateral frontal cortical regions showed
impaired temporal context memory (Kopelman et
al. 1997)
 Working memory (planning, organization of
material, monitoring of responses, inhibition of
inappropriate responses) deficits are reported.
 Emotional memories: Humans form more vivid
memories of emotionally arousing events rather
than neutral events.
 Lesion in the basolateral nucleus (BLA) of
amygdala (a major out put pathway, the stria
terminalis), can prevent the facilitation of
memory produced by emotional arousal. (McGough
2000)

53.  D/MTL lesions: less likely to respond to specific
cues suggesting a more fundamental amnesic
defect;
 D/MTL leison : more impairment in recall but not
in recognition testing.(Aggleton and Shaw 1996)
 Recognition memory and familiarity
judgments may be impaired in damage to
perirhinal cortex.
 However findings are overlapping with the
amnesia found in TL and Diencephalon
lesions.

54.  A patient with damage in vicinity of Sylvian fissure
had markedly reduced STM as evidenced by digit
span and verbal list memory dysfunction.
 LTM was retained. (Shallice and Warrington 1969)
 Brodmann’s area 40 damage (supramarginal gyrus
especially on left side) is known to cause
impairment in verbal STM.
 Patients with lesions in the right parieto occipital
areas have difficulties in visuo-spatial working
memory tasks.
 These correspond with the components of theory
of WM.

56.  Implicit memory
 Various studies have shown that D/MTL/F
patients do not have implicit deficits.
 Procedural memory-Cerebellum,Basal
ganglia,cerebral cortex
 This is seen in patients with subcortical
dementias and basal ganglia lesions such as in
Parkinsonism and Huntington’s disease. (Heindel
et al 1998)
 Parkinsonism patients also have impaired habit
learning. This implicates the neostriatum.
 Priming is also dependent on cortical regions.
(Shimamura 1986)
 Visuoperceptual priming depends on integrity of
occipital circuits. (Keane et al 1995)
 However when the difficulty level of the priming
task is increased, MT/D structures come into
play.

57.  Conditioning :
Classical conditioning
 Discrete behavioural responses – Cerebellum
 Emotional response – Amygdala
 Working Memory
 Central executive: frontal lobes
 Visiospatial sketch pad: Neocortex
 Phonological loop: perisylivian region
 Semantic memory:
 It involves a profound loss of semantic
knowledge; involves profound loss of meaning,
encompassing verbal and non-verbal material
and resulting in severe impairments in naming
and word comprehension.

58.  Supposedly controlled by the left infero-lateral
temporal lobe. (Patterson and Hodges 1995)
 Episodic memory- Hippocampus,Mammillary
body.Diencephalon,Frontal lobe
 Temporal gradients in memory loss:
 Ribot’s law (1882): progressive destruction of
memory follows a law that most recent
recollections are the weakest and hence go
first.
time
Trauma
Episodic
memories
Retrograde
Amnesia
Anterograde
Amnesia

59.  Studies have shown that-
 Steep temporal gradients occur in pure amnesic
syndromes such as those that implicate D/MTL.
 The slope is gentle in dementia and other
global lesions and frontal lobe lesions.
 Implication: MTL and D are critical to initial
memory formation and also in consolidation
of memories of 2-3 years or longer, after
which the memories are stored in neocortex
and no longer dependent on these
structures.

60.  Visual memory: There are 2 streams that are
activated on visual memory tasks.
 Ventral stream/ occipito-temporal stream:
essential for identifying objects.
 Dorsal stream/occipito-parietal stream:
appreciation of spatial resolution among
objects.
 There are specialized processing areas with in
the processing streams such as those for
perception of color, shape and faces.
 Prefrontal areas have also been found
activated with visual memory tasks.

61.  Priming: decrease in activity in occipito-
temporal cortex of the ventral stream. This
may be an evolutionary advantage in that
being surrounded by familiar stimuli may
cause less energy expenditure.
 Perceptual and motor skill learning: leads
to an expansion in the cortical
representation along with a decrease in
representations in cerebellum and
prefrontal cortex as the skill is being
learnt.
 Thus the PFC and cerebellum may be
preferentially recruited into learning of a
new skill but when through repetition, it
becomes automatic and localised in the
neocortex.

62.  In studies where novel stimuli is used, the initial
points of activation are the hippocampus, this is
especially so with visual stimuli.
 Verbal material is mostly familiar and does not
activate the hippocampus.
 Novel Semantic Memory Retrieval Is Episodic
Memory Encoding-The verb generation task and
the noun repetition task perform two functions
concurrently.
 Encoding and Left Prefrontal Activation
 Retrieval and Right Prefrontal Activation
 Hemispheric encoding/retrieval asymmetry in
episodic memory (HERA):(Tulving et al. 1994).

63.  (i) The HERA model asserts that the left and the right
prefrontal cortical regions are differentially involved
in episodic and semantic memory processes.
 (ii) Left prefrontal cortical regions are involved in
retrieval of information from semantic memory to an
extent that right prefrontal areas are not, at least
insofar as verbal information is concerned.
 (iii) Left prefrontal cortical regions are involved in
encoding information about novel happenings into
episodic memory to an extent that right prefrontal
areas are not, at least insofar as verbal information is
concerned.
 (iv) Right prefrontal cortical regions are involved in
retrieval of episodic information to an extent that left
prefrontal areas are not.
 (v) Right prefrontal cortical regions are involved in
retrieval of episodic information to an extent that
does not hold for retrieval of semantic information.

64. Synaptic change in Memory:
Neuronal plasticity (Kandel 1991)
Neurons can show history-dependent
behavior by responding differently as a
function of prior input, and this plasticity of
nerve cell and synapse is the basis of
memory
Short lasting plasticity – increase in
neurotransmitter release and specific
synaptic events
Long lasting plasticity – New protein
synthesis,physical growth of neural
processes and increase in number of
synaptic connections

65.  LTP is observed when a postsynaptic neuron is
persistently depolarized following a brief burst
of high frequency stimulation.
 The phenomenon of LTP is a candidate
mechanism for mammalian long-term memory.
 Hippocampus- Dentate gyrus, CA1,CA3
 Cerebral cortex- Visual, Somatosensory,Motor
Prefrontal
 Amygdala
 Nucleus acumbens
 Ventral tegmental area
 Thalamus
 Striatum
 Cerebellum

66. Model for the induction of long-term potentiation
(LTP). During normal synaptic transmission (left), synaptically
released glutamate acts on both NMDA and AMPA receptors. Na
flows through the AMPA receptor channel but not through the
NMDA receptor channel because of the Mg2 block of this channel.
Depolarization of the postsynaptic cell (right) relieves the
Mg2 block of the NMDA receptor channel and allows Na and
Ca2 to flow into the cell. The resultant rise in Ca2 in the dendritic
spine is a necessary trigger for the subsequent events leading
to LTP.

67. Model for sequence of events leading to structural changes following
triggering of LTP. Within 10 minutes of LTP induction, AMPA receptors
are phosphorylated and inserted into the postsynaptic membrane. This
process leads to an increase in the size of the postsynaptic density
(PSD) and the production of perforated synapses within 30 minutes. By
1 hour, some perforated synapses split and form multispine synapses.
Eventually, retrograde communication, perhaps involving cell-adhesion
molecules, leads to presynaptic structural changes and the production
of new synapses.

68. Properties of LTP:
 Established quickly and lasts for a long time
 Associative i.e co-occurence of presynaptic
activity and postsynaptic depolarization,
Occurs only at the potentiated synapse, not
at all synapses terminating on the
postsynaptic cell.
 The induction of LTP is mediated post-
synaptically and involves activation of NMDA
receptors, which permit influx of calcium
into post-synaptic cell.
 LTP occurs prominently in the hippocampus.

69. Long term depression:
 Refers to “use dependent long-lasting decreases in
synaptic strength (Linden et al. 1995)
 Work in parallel to LTP with respect to memory
functioning.
 It may help to reset synapses that have been
potentiated by LTP, serve as a cellular mechanism of
forgetting, form active inhibitory system to attenuate
signals from adjacent potentiated synapses, form
active inhibitory system to attenuate signals from
adjacent potentiated synapses.
(Tsumoto 1993)

70. Model for the signaling cascades responsible for LTD and LTP. LTD is
generated when a low rise in Ca2 binds to calmodulin (cam) and
activates calcineurin (PP2B). Calcineurin then dephosphorylates
inhibitor 1 (I1), which therefore no longer inhibits protein phosphatase
1 (PP1). Active PP1 may act on any number of substrates including
camkii or AMPA receptors (left). LTPis generated when a high rise in
Ca2 activates camkii. Other protein kinases that may also be involved
in triggering LTP are protein kinase C (PKC), cAMP-dependent protein
kinase (PKA), the tyrosine kinase src (Src), and MAP kinase
(MAPK)(right).

71.  Evidences are based on neuroimaging and
neuropsychological studies. Linden and Connor
1995
 Glutamate: Two types of glutamate receptors
a) Linked to ion channel (NMDA, AMPA, and
kainite):
Induction of LTP is mediated post-synaptically and
by activation of NMDA receptor leading to influx
of calcium into the postsynaptic cell; increases the
pre-synaptic release of neurotransmitter and
increase in the number of postsynaptic receptors.
b) Linked to G- protein (metebotropic receptors):
—mediate LTP

73.  In mice, by selective deletion of NMDA receptors
in the CA1 field of hippocampus, many aspects
of CA1 physiology remain intact, but the
CA neurons don’t exhibit LTP and memory
impairment is observed in behavioral tasks.
 Glutamate antagonists are beneficial in
Alzheimer’s and vascular dementia (prevents
glutamate excitotoxicity related
neurodegeneration) e.g. memantine

74. Norepinephrine:
 Postsynaptic 2 adrenoceptors has role in
prefrontal cognitive functions.
 Infusion of 2 agonist Guaifencine into the
prefrontal cortex of monkey improves working
memory performance and infusion of 2
antagonist Yohimbine into monkey prefrontal
cortex impaired the working memory
performance.
 Administration of high dose of 1 agonist
Cirazoline improved working memory by
activating PFC, but adminstration of 1
antagonist Prazosin had no effect on working
memory

75. Acteylcholine:
Deficiency in cholinergic functioning, due to
degeneration in cholinergic projections from the
nucleus basalis of meynert in Alzheimer’s dementia.
Beneficial effect of acetyl cholineesterase which
increases the ACh level e.g Donepezil, Rivastigmine
and Galantamine in Alzheimer’s disease.
Dopamine:
Regulates excitability of cortical circuitry upon which
the working memory function of PFC depends.
It also plays role in LTP (LTP can be blocked by
dopamine receptor antagonist)

76. Other peptides and hormone:
Glucocorticoids: Activation of adrenal steroid
receptors in the hippocampus play role in
memory storage, also via amygdala.
Opioids: Opioid agonists impair memory and
opioid antagonists enhance memory.
GABA: Antagonist enhances memory and
agonists impair memory

77.  Wechsler Adult Intelligence Scale Revised
(WAIS-R)
 Wechsler Memory Scale- Revised (WMS-R)
 Halstead Reitan Neuropsychological Battery
(HRNB)
 Rennick Repeatable Battery
 Stroop Colour Word Interference Test
 P.G.I. Memory Scale:

78.  Memory is distributed and localized; Temporal lobe
and diencephalon have role in explicit memory;
Neocortex, cerebellum and basal ganglia have role
in implicit memory
 Synaptic changes are important for memory
processing
 Neuropsychological perspectives have been
limiting, implying sharp compartmentalization
 In-vivo imaging indicates a more dynamic and
integrated functioning.

79.  Different processes of memory are not being
separated clearly by imaging studies
 Substantial overlap between different types of
amnesia indicates that demarcation of functions
may not be as sharp as thought earlier
 PET Scan and fMRI are useful in further study
 There is a significant role of interconnecting
regions that needs to be looked into.

80.  Study repeatedly to boost recall
 Spend more time rehearsing or actively thinking
about the material
 Make material personally meaningful
 Use mnemonic devices
 associate with peg words--something already stored
 chunk information into acronyms
 Study in spaced intervals
 Activate retrieval cues--mentally recreate situation
and mood
 Minimize interference
 Test your own knowledge
 to rehearse it
 to determine what you do not yet know