Memory is the ability toMEMORY

conscious or recall stored

retention unconscious
and
and
level. It is the past events at the
storage form of the relatively permanent
Forms of Memory learned
Memory is divided
information.
and into:
non-declarative (or
declarative (or explicit
major differences memory)
implicit/reflexive
between
96.2. the two memory). The
are
given in Table
Types of
Declarative Memory
Depending
divided
on how
long a
conscious memory lasts, it is
memory.
broadly into two
major types: recent and remote
1. Recent or short-term
mediating inmmediate memory: It involves
recall of events thatmechanisms
seconds to
hours before. It is lost occurred
certain neurological disorders. in individuals win

NOTrE
When it occurs for
very short
working memory. For example, toperiods
it is
named
number before dialing. look up a telepno

2. Remote or
long-term memory: It involves me
mediating memory of the emote (distant) past It
It
nce o f
b

remarkably resistant and persists in the pres

severe brain damage.

O NOTE
Factors influencing conditioned reflexes basedleamins
memory ( * t
1S a classical example of non-declarative me
to above).
 Ch. 96: Higher Functions of the Nervous System 935

Table 96.2:
Differences between two major forms of memory
Declarative (explicit) memory
Non-declarative (implicit) memory
the
for the
It isfor
real knowledge about people, place and things.
1. 1. It is important for training reflexive motor or
perceptual
skills.
2 Types: 2. Types:
aSemantic memory for facts (e.8. words, rules and
languages)
(1) Procedural memory for skills and habits
(i) Priming memory: for
(i) Episodic memory for events recognition of words or objects
3.It is associated with consciousness of awareness
3. It does not involve consciousness/awareness and is largely
unconscious (reflexive)
tis dependent on the hippocampus and parts of the medial 4. It does not involve
temporal lobes of the brain for its retention. processing in the hippocampus.
Note: Declarative (explicit) memories that are
initially required for
memories once the task is thoroughly learnt. learning activities can become non-declarative (implicit)
Physiology of Memory
(1) are anaesthetized,
[tis based on certain clinical and experimental observations.
(i) given electroshock treatment,
Example 1. Stimulation of certain portions of the (ii) subjected to hypothermia, or
temporal lobe produces detailed memories of events iv) treated with antibiotics that inhibit protein synthesis.
that occurred in remote past, often beyond the
power Such a treatment 4 hours after the
of voluntary recall. A particular memory is generally training session has
no effect on the memory acquisition.
produced by stimulation of a definite area. It unfolds
This shows that there is of
as long as the stimulus is applied and stops when the a
period encoding or

stimulus is discontinued. consolidation of memory during which the memory trace

is liable to injury. Following this period, a stable and
However, these areas in the temporal lobe have not
remarkably resistant memory develops.
been proven, since stimulation of temporal lobe or
patients with temporal lobe disorders generally manifest
with epilepsy.
ONOTE
Biochemical events involved in memory are the same
Thus it seems unlikely that the memories themselves asalready have been decribed for learning.
are localized in the temporal lobes. Instead, the temporal
lobe points are probably keys that unlock memory traces The working imagination processing and memory
Stored elsewhere in the brain and the brain stem. Normally, refer to Fig. 96.5.
a key is turned by some sort of comparing, associating
when there is a similarity between the memory and Mechanism of declarative memory encoding
crcut
ne Current sensory input or a stream of thought. It is a There is considerable evidence that the encoding process
ommon experience, the memory of an intese scene can be involves the hippocampus (and its connections) and
neighbouring cortex viz. entorhinal, perirhinal and
the
produced not only by a similar scene but also by a sound
uf Smell associated with the scene. (deja Vu phenomenon), parahippocampal areas. These connections contain cell
the French words means already see1. bodies and fibers of the cholinergic system. However,
glutamic acid also play an important role (page 944).
xanple 2. There is frequently a loss of memory
tne events immediately before brain concussion or Proof
rOshock therapy. This phenomenon is termed as 1. Bilateral destruction of the ventral lhippocampus in humans
from few hours to or animals that destroys
rdne amnesia, which persists cholinergic neurons produces
years,but remote memory is not affected. (Concussion striking defects in recent memory with intact remote
memory. In addition, they cannot form new long-termn
Stransient loss of consciousness resulting from a
head injury.) memories.
Examp 3. In animals, acquisition (gaining and 2. Stimulation of hippocampus with chronically implanted
storation) of learned:responses is prevented if within 5 electrodes in humans which produce seizures is
often
ts alter each training session, the animals: associated with loss of recent memory.
 936 Unit X: The Nervous
systemn
The response does not persist n the regenerat
Motor Short-term
memory bulffers if the worm is exposed to ribonuclease, an rated
Cortex
destroys RNA.
enzyme that

Mechanism

Discharge of neuron during learning session could

to changes which increase mRNA synthesis and ad
increase synthesis of particular proteins. These
Prefrontal cortex: could modify synaptic transnission by affecting: proteins
Working memory
() transmitter synthesis
(i) membrane permeability, or
Hippocampus:
Episodic memory (ii) some other neural processes.
significant memory
Cerebellum:
Amygdala: Procedural Drugs That Facilitate Memory
Emotional memory
memory Various CNS stimulants can improve learning in animals
Automatic
when administered immediately before or after the
nemory
learning sessions. These agents act probably by facilitatine
Fig. 96.5 The working imagination processing and memory consolidation of memory trace. The molecular or cellular
change that takes place somewhere along the neural
3. Chronic alcoholics with brain damage develop pathways is called the memory trace. The agents that
considerable impairment of recent memory,
correlates well with the presence of pathologic changes
which facilitate memory include:

() Caffeine.
in the mammillary bodies, a major site of projection
(i) Physostigmine. It inhibits acetyl-cholinesterase and
for hippocampal fiber. hence breakdown of A-ch.

(ii) Amphetamine.
IMPORTANT NOTE (iv) Nicotine. It stimulates nicotinic cholinergic receptors.
Severaldrugs that impair memory or alter recent (v) Pemoline (cylert). It also stimulates the RNA
in the
memory produce abnormal discharges synthesis.
hippocampus. (vi) Convulsants e.g. picrotoxin, strychnine and pentylene
tetrazol (Metrazol).
Protein Synthesis and Memory
resistance to
Nature of stable memory is unknown, but its ALZHEIMER'S DISEASE AND
electroshock and concussion suggests that memory might SENILE DEMENTIA
be stored as a biochemical change in the neurons. There Alzheimer's disease is characterized by progresstoelos
and activation of genes
is evidence that protein synthesis memory and cognitive function (page 922) in middle aged
is involved in some way in the processes responsible for individuals. Thus the condition is frequently associate
memory. with:
1 memory failure for recent events
Evidences with los
in nerve cells (1 lack of spontaneous activity and initiative
1. In rats, increased RNA synthesis occurs
of intellectual functions
subjected to intense stimulation.
(11) extrapyramidal and akinetic hypertonic symptou
2. In experimental animals, administration of drugs which
inhibit protein synthesis, such as puromycin, acetoxy (page 895)
(iv) loss of spatial orientation (page 915).
cycloheximide etc. disrupts recent memory.
Hel

to retain learned After 2 or 3 years, dementia (memory loss) becon aphuasad

3. The ability of regenerated planarians established and focal symptoms occur, such as
habits. Planarian are flat worms with rudimentary to perform volunt

nervous system and a

remarkable ability to regenerate (speech disorder),apraxia (inability objects
i

when cut into pieces. They

can be taught to avoid movements) andagnosia (inability to recognize
trained worm is divided spite of intact sensory modality).
certain visual stimuli. If a
e called

the worm regenerated from the Similar features in the old age (over 65 years
into two, not only does
head piece retains the response but from the tail also. senile dementia.
 Ch. 96: Higher Functions of the Nervous System 937

The sequence of events in the affected neurons

Mutation of amyloid precursor prolein gene
Parietal cortex
Aggregation of B-amyloid peptides
Frontal cortex
Formation of extracellular plaques
(Senile plaques: toxic polypeptide)

Inflammatory reaction with oxidative damage

Hippocampus Altered nerve fibers and reactive

Septal nuclei- glial cells (Gliosis)

Formation of intracellular neurofibrillary tangles

Degeneration of cholinergic neurons in the cerebral
cortex and hippocampus

(A) Alzheimer's disease

(B)

Fig. 96.6 The major cholinergic pathways

involved (A) and pathogenesis (B) in Alzheimer's disease

Pathogenesis: Both the conditions are caused by

NOTE degeneration of cholinergic nerve terminals in the cerebral
of age and
10-15% of the population over 65 years cortex and hippocampus (Fig. 96.6). There is a severe
of
50% of population over 85 years have some degree loss of cholinergic neurons in the nuclei of septal region
dementia. of the forebrain that forms a major source of cholinergic
innervation of the cerebral cortex.