Memory Flashcards

1
Q

What is Santiago Ramon y Cajal’s theory of memory storage?

A

That memories are stored via physical changes to neurons.

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2
Q

What is Holger Hyden’s RNA theory of memory?

A

That in order for there to be physical change to neurons, there must be gene transcription, RNA and protein production.

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3
Q

What 3 conditions must be met according to Hebbian theory in learning?

A
  1. Homosynaptic plasticity: the strengthening event and synaptic strengthening must occur at the same time
  2. Association: the firing of the pre and post-synaptic neurons must be closely correlated in time
  3. Input specificity: the connection must be distinct from the other 50,000 connections each neuron has
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4
Q

What did work by a) Seymour Benzer and b) Eric Kandel demonstrate about short-term memory?

A

a) That it involves signal transduction cascades (created drosophila mutants)
b) That it involves existing enzymes to increase NT release (worked on sea snails)

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5
Q

What is the signalling cascade in short-term memory? Use 5HT transmission as an example.

A

5HT binds its GPCR. The GPCR activates adenylate cyclase. Adenylate cyclase causes the formation of cAMP. cAMP activates PKA. PKA increases NT release.

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6
Q

Long term memory requires RNA synthesis. This was demonstrated in work by Seymour Benzer on drosophila. What difference is there in the signalling cascade in short and long-term memory?

A

In LTM the cascade is the same, with the addition that PKA’s catalytic subunit 5L translocates to the nucleus and phosphorylates genes, causing transcription. This causes lasting effects by permanently increasing NT release.

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7
Q

There are 2 types of memory. What are they?

A
  1. Declarative: memories can be expressed, e.g. episodic or semantic.
  2. Non-declarative: memories are procedural (non-verbal)
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8
Q

What are the 4 stages in memory?

A
  1. Acquisition
  2. Consolidation
  3. Retrieval
  4. Extension
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9
Q

Describe memory acquisition.

A

STM is encoded by the hippocampus.

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10
Q

Describe memory consolidation.

A

There are 2 stages: first there is synaptic consolidation, or strengthening, in the hippocampus. Secondly there is systems consolidation whereby the memory trace is transferred to the neocortex for storage. In consolidation, STM becomes LTM.

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11
Q

When can the process of consolidation be observed?

A

During sleep in the phenomenon of replay, e.g. place cell activity.

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12
Q

What is the basis of memory extension?

A

Multiple trace theory: each time you are presented with information, the memory is neutrally encoded in a unique memory trace which is a combination of its attributes.
Basically each time you encounter something, the memories of that encounter are added to the catalogue of memories you already have of that thing.

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13
Q

How is memory organised in the brain?

A

Synapses are the outputs of memory, thus memory circuits are distributed around the brain.

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14
Q

A memory involves only a single synapse. True or false?

A

False: a single memory involves multiple synapses.

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15
Q

What evidence is there for numerous mechanisms acting in memory formation?

A

New memories can be made in under a second, and some memories last for years.

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16
Q

STM involves existing enzymes to modulate NT release, showing that in STM existing synapses are modified. How do we know new synapses are not created in STM?

A

A new synapse cannot form in under a second, as new memories can.

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17
Q

If synapses are the outputs of memory, strengthening a synapse will increase its output and thus the strength of the memory trace. List 3 ways in which this can be achieved.

A
  1. Increasing the no. of post-synaptic receptors
  2. Changing the properties of the receptors
  3. Increasing neurotransmission
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18
Q

What are the 2 major NTs involved in memory formation?

A
  1. Glutamate: main excitatory transmitter that causes rapid depolarisation.
  2. GABA: main inhibitory transmitter that causes hyperpolarisation by causing Cl- influx.
19
Q

Which of glutamate’s 4 receptors is involved in memory?

A

The NMDA receptor.

20
Q

What is the NMDA receptor involved in?

A

Na+ influx (generation of APs) and Ca2+ (NT release).

21
Q

How does glutamate act on the NMDA receptor in order to facilitate memory augmentation?

A

When glutamate binds NMDA it causes the Mg2+ ion blocking the channel to move. This allows Na+ into the cell causing rapid depolarisation. The generation of an AP opens Ca2+ channels. The Ca2+ influx acts on AMPA receptors (fast glutamate receptors), either causing an increase in their number or changing the properties of the synapse.

22
Q

AMPA glutamate receptors are incredibly fast. How quickly can they respond?

A

In 1-2ms.

23
Q

Ketamine blocks NMDA receptors. What effect does this have on memory?

A

It causes memory loss, i.e. when you are under the influence of ketamine you cannot properly form/augment memories, so when it wears off you can’t remember what happened.

24
Q

How does ketamine block the NMDA receptor?

A

It acts as a non-competitive inhibitor to glutamate.

25
Q

Describe how a non-competitive inhibitor works.

A

It binds to the receptor in a different place to glutamate, but causes a conformational change so that glutamate can no longer bind to the receptor site.

26
Q

Ketamine mimics the Mg2+ ion blocking the pore in the NMDA receptor. True or false?

A

True.

27
Q

What is MK801?

A

A less reversible alternative to ketamine.

28
Q

What are APS and AVS?

A

Competitive inhibitors to glutamate.

29
Q

APS and AVS have their greatest effects when injected peripherally. True or false?

A

False: they have no effect when injected peripherally as they cannot cross the blood-brain barrier.

30
Q

What drug class does ketamine fall in to?

A

The dissociatives: this is a class of hallucinogen that distorts both sensation and perception, giving a feeling of detachment as it block neurotransmission.

31
Q

What does ketamine do to a user?

A

Puts them in a semi-awake state of analgesia, producing a trance-like state of catatonia.

32
Q

What sensations are common when using ketamine?

A

A sense of leaving the body, a loss of time etc.

33
Q

Which GABA receptor is involved in memory?

A

GABA-A: this is a fast ligand-gated channel, as opposed to GABA-B which is a GPCR.

34
Q

Which molecule does GABA-A allow into the cell?

A

Cl- in hyperpolarisation.

35
Q

GABA-A receptors are found throughout the body. True or false?

A

False: GABA-A receptors are localised to the brain.

36
Q

How many peptides make up the GABA-A receptor?

A

5.

37
Q

Which drugs act on GABA-A receptors. What effects do they have?

A

Benzodiazepines prevent memory consolidation.

38
Q

What are benzodiazepines?

A

Anxiolytics.

39
Q

How do benzos prevent memory consolidation?

A

Benzos enhance GABA action in allosteric modulation, which means there is an increased effect for the same amount of NT. This creates a tendency for hyperpolarisation, thus reducing synaptic transmissions. Synapses are not strengthened.

40
Q

What effects do benzos have on the body? How?

A

Sedative/hypnotic and muscle relaxation by increasing GABA action, i.e. inhibiting neuronal over-activity that leads to anxiety.

41
Q

Benzos were developed as an alternative to the barbiturates of the 1900s. What was wrong with the barbiturates?

A

They were hugely addictive and often lethal, as their effects were additive.

42
Q

Give some examples of benzos.

A

Synthetic: librium and diazepam (Valium)
Natural: St John’s Wort

43
Q

It is said that using benzos for a prolonged period of time can create dependence. How long is this period?

A

Over 1 month of usage can create dependence.