Memory

Question 1

Learning

Answer 1

• The process by which we acquire new knowledge.

* How experience changes the brain and behaviour

Question 2

Memory

Answer 2

• The process by which we retain knowledge over time
• How that knowledge is stored and retrieved / reactivated (and of course impact on behaviour)
• Amnesia
• Any pathological loss of memory function

Memory sits largely in the domain of cognitive psychology and its ‘information-processing’ approach.
Cognitive psychologists equate mental
processes to the software installed on a
computer and the brain to the hardware

Question 3

Terminology

Answer 3

> . Sensory Memory: a brief memory store holding incoming sensations and perceptions (pre-attentive).

> . Short-term Memory (STM): Holds 7+/-2 items that have been attended to. What we are conscious of.

> . Long-term Memory (LTM): The neural “warehouse” storing information for long periods of time (hours / years).

Question 4

LTP Process

Answer 4

1) Induction
>. Second messenger kinases are activated by an influx of Ca++ following depolarization: a postsynaptic event
2) Maintenance
>. Depends on the enhancement of neurotransmitters: a presynaptic event
>. Thus for LTP to occur a message must be sent from the postsynaptic to the presynaptic neuron, a problem for the unidirectional transmission doctrine

Question 5

Hebb’s (1949)

Answer 5

Model of the neural mechanism of memory argued that enduring changes in the efficiency of synaptic transmission were the basis of LTM.
Bliss and Lømø (1973) first demonstrated long-term potentiation (LTP) in the laboratory.
LTP prominent in structures associated with learning and memory, and operant learning produces LTP-like changes in hippocampus:
Mutant mice with little hippocampal LTP learn Morris Water Maze very poorly

Question 6

Post-traumatic amnesia

Answer 6

> . 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.

Question 7

Amnesia and Electro-convulsive Therapy (ECT)

Answer 7

Water-deprived rats placed in an empty test box for 10 mins on 5 consecutive days. Box contains a small ‘niche’.
6th day – water spout in niche – allowed 15 secs to drink. At 10 secs, 1 min, 10 mins, 1 hour, or 3 hours after, each rat received an electroconvulsive shock.
Question is, how long does consolidation take?
10 min test session next day showed a significant difference at 10 mins.

Question 8

Memory & Amnesia

Answer 8

Memory is a complex phenomenon, that appears to
involve multiple structures: Hippocampus – spatial location
Perirhinal cortex – object recognition
Mediodorsal nucleus – Korsakoff’s symdrome
Basal forebrain – Alzheimer’s disease
Pre-frontal cortex – attentional functions
Amygdala – emotional learning / fear learning

Question 9

Encoding and Consolidation

Answer 9

The hippocampus encodes and stores declarative memory for a limited duration. These memories are
gradually encoded in other regions of the brain for more permanent storage. Consolidation: a neurophysiological process that results in structural changes in the cortex via long-term potentiation (LTP)

Question 10

LTP: Part 1

Answer 10

• LTP depends on the coincident firing of neurons
• Glutamate (an amino acid) is the main neurotransmitter in the hippocampus
• There are two kinds of glutamate receptors:
1) NMDA (N-methyl D-asparate) receptors
2) Non-NMDA receptors
• Non-NMDA receptors dominate as NMDA receptors are usually blocked by magnesium.
It becomes unblocked only when
the postsynaptic cell is depolarized

Question 11

LTP: Part 2

Answer 11

• To activate the NMDA receptors not only must glutamate be ready to bind but the post-synaptic cell must be depolarized
• The resulting calcium influx into the postsynaptic cell through the unblocked NMDA receptor channel initiates LTP through activating “energizing” enzymes
• These enzymes are called “kinases” and are second messengers:

First messengers: neurotransmitters (e.g., 5-HT)
Second messengers: chemicals that relay information from within the cell
•The rise in Ca++ in the cell activates a second messenger (calpain) which causes a retrograde signal to be sent from the post- to presynaptic cell
• This retrograde signal must diffuse across the post- synaptic memory and across the synaptic cleft to receptors on the presynaptic cell
• The best candidate thus far is nitric oxide (NO)