Memory

Question 1

What is declarative memory?

Answer 1

Involves the formation and retrieval of explicit memories and facts and events specific to an individual and involving the CONSCIOUS RECOLLECTION of past events

Question 2

What is non-declarative memory?

Answer 2

DOES NOT REQUIRE CONSCIOUS RECALL
May involve skills, category, priming, associative (operative/pavlovian), or non-associative (habituation)
- associative conditioning → Pavlov’s dogs: create an association between two stimuli
- operant conditioning - Skinner’s box

Question 3

What may declarative memory be divided into?

Answer 3

Semantic or episodic

Question 4

Describe semantic memory

Answer 4

recollection of information not associated with time or place, but relating more to
meaning and function (eg. of objects, words); also dependent on medial temporal lobes,
particularly the anterior and lateral regions of the left hemisphere
FACTS AND GENERAL KNOWLEDGE

Question 5

Describe episodic memory

Answer 5

recollection of specific events occurring at a particular time and place; involves the
medial temporal lobe, including the hippocampus, perirhinal cortex, and parahippocampal cortex,
as well as prefrontal cortex
PERSONALLY EXPERIENCED EVENTS

Question 6

What areas are important in non-declarative memory?

Answer 6

Corticostriatal system, motor cortex and cerebellum

Question 7

What is a Hebbian synapse?

Answer 7

‘Cells that fire together wire together’ → increase in synaptic efficacy arises from a presynaptc cell’s repeated and persistent stimulation of the postsynaptic one

Question 8

Example of a Hebbian synapse

Answer 8

LTP at the synapses between hippocampal

CA3 Schaffer collaterals (Scs) and CA1 cells is Hebbian

Question 9

What are the two types of glutamate receptor on hippocampal CA1 cells and what are their basic roles?

Answer 9

NMDA → induction

AMPA → maintenance

Question 10

What are the 6 main symptoms of Korsakoff’s?

Answer 10

1. Anterograde amnesia
2. Retrograde amnesia, severe memory loss
3. Confabulation, that is, invented memories which are then taken by the patient as true due to gaps
   in memory, with such gaps sometimes associated with blackouts
4. Minimal content inconversation
5. Lack ofinsight
6. Apathy - the patients lose interest in things quickly, and generally appear indifferent to change

Question 11

Which form of memory has LTP been implicated in at the hippocampus?

Answer 11

Declarative → both spatial (remembering environmental cues) and behavioural (inhibitory avoidance)

Question 12

Describe LTP mechanism

Answer 12

1. The arrival of an AP at the terminal of an excitatory pre-synaptic neuron causes glutamate release into the synaptic cleft → diffuses → binds to AMPA and NMDA Rs on post-synaptic membrane
   - 2. AMPA Rs open → Na+ influx and depolarisation of the neuronal membrane
2. At rest, NMDA Rs have a Mg2+ ion in the channel pore, preventing the passage of ions, this glutamate binding elicits no effect
3. However this Mg2+ residence is voltage-dependent: hence AMPA R activation which causes depolarisation of the neuronal membrane, will cause Mg2+ to leave the channel, enabling glutamate binding to open the channel
4. Opening of the NMDA R by glutamate binding → Na+ and Ca2+ influx → rise in [Ca2+] i → activation of 2 important kinases:

o The Ca2+/calmodulin dependent protein kinase II (CaMKII) → phosphorylates and
activates existing AMPA Rs in the post-synaptic membrane, increasing their
responsiveness to glutamate

o Protein kinase C (PKC) → phosphorylates NMDA Rs, reducing the Mg2+ blockage and
hence causing them to be more responsive to smaller depolarisations

o Both kinases stimulate AMPA R trafficking to the membrane

Question 13

How may chanegs to the pre-synaptic neuron also occur during LTP?

Answer 13

Release of retrograde messengers from the post-synaptic neuron → act presynaptically

Question 14

Why can changes in early LTP not last?

Answer 14

as protein phosphorylation is not permanent
and even the protein molecules themselves are not permanent and undergo a process of
turnover – hence other processes must occur that allow long-lasting synaptic enhancement.

Question 15

Describe late-LTP

Answer 15

driven by protein synthesis and
changes in gene expression

This protein synthesis is initiated by the protein kinases at play during early-LTP, which
function by activating transcription factors such as CREB, which stimulate the expression of
other proteins.
- Although most of these newly synthesised proteins have not yet been identified, they
include other transcriptional regulators, protein kinases, and AMPA Rs
- The roles of these proteins is not clear, but one outcome appears to be an increase in the
number and size of synaptic contacts during LTP, which serves to make LTP essentially
permanent