Memory 2 - Consolidation Flashcards

1
Q

What are the 3 stages of visual memory?

A
  • Iconic
  • Short term
  • Long term
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2
Q

What is iconic memory?

A

An immediate, but very short lasting retention of visual information, lasting no longer than one second.

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3
Q

What is visual short term memory?

A

A more long lasting form which keeps images active for processing within the visual cortical neurons.

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4
Q

What is visual long term memory?

A

Allows us to remember and recognise visual stimuli for as long as an entire lifetime.

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5
Q

What is the mechanism behind iconic memory?

A

Mechanisms in the eye, e.g. the retina. The brightness of the stimuli seems to leave an imprint on the retinal systems, causing the image to remain much like the after-effect of a camera flash causes.

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6
Q

What is the mechanism behind visual short term memory?

A

Sustained neural activity in the inferior temporal cortex which causes the image to remain for several seconds.

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7
Q

What is the mechanism behind visual long term memory?

A

No concrete findings as yet. Patients with sever temporal lobe damage suffer from amnesia, characterised by impairments in visual recognition memory..

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8
Q

What is repetition suppression?

A

The reduced cortical/neuronal response when an object is recognised from long term memory. (Fahy et al., 1993; Meister et al., 2005; van Turennout et al., 2000).

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9
Q

Which type of memory did Sperling’s array test?

A

Iconic memory

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10
Q

What was found from Sperling’s array experiment and how can this be explained?

A
  • That participants could remember a greater percentage of the letters (75%) in partial report conditions, but only 35-40% in the full report condition.
  • That, if participants are asked at a 1 second delay, the advantages of the partial report are lost, with accuracy dropping back down to 35-40%.

This can be explained by the 1 second duration of iconic memory. In the full report conditions, only 4/5 letters can be reported before the visual memory/representation of the image decays. In the partial reports, pps could report a large percentage of the line, as there were less letters, before their memory for it decayed.
However, when the questions were delayed by a second, the representation had decayed before they could report more than 40%.

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11
Q

What does perceptual learning relate to?

A

Learning of perceptual information, such as visual stimuli.

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12
Q

What does procedural memory relate to?

A

Memory for skills and/or processes. E.g. riding a bike, making a tea, etc.

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13
Q

What is the mnemonic function of a neuron?

A

Memory processing ability of a neuron

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14
Q

True or false: there is a clear distinction between perception and memory.

A

False: there is no clear distinction yet, between perception and memory, reinforcing the notion that memory is a fundamental process that underlies other functions in the brain.

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15
Q

What is associative learning?

A

Learning that involves the formation of links between stimulus and response. (Pavlovian conditioning)

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16
Q

What is instrumental learning?

A

Learning to produce behaviours to bring about a desired effect/event. e.g. the rat pressing the lever for food.

17
Q

What is the function of consolidation?

A

To enable a memory to be stabilised into a long term form.

18
Q

How can the lack of spatial resolution in patient studies be made up for?

(e.g. how can we get around the fact that multiple brain areas are often damaged/removed, meaning we cannot always reliably attribute impairments to one or two brain areas alone?)

A

We can ensure we test a very large sample and then correlate the extent of damage to a specific target area with the impairments that we observe.

19
Q

What is Urbach-Wiethe disease?

A

A degenerative disease which results in neuronal cell death in both sides of the amygdala.

20
Q

Why does Urbach-Wiethe disease occur?

A

Genetic disorder which causes the build up of calcium deposits in the amygdalae, leading to neuronal cell death in affected areas.

21
Q

Are there any diseases which specifically target and damage only the amygdala? If so, what are they called?

A

Urbach-Wiethe disease.

22
Q

What is aspiration?

A

A method of causing damage to a specific area of the brain, which involves sucking out parts of the brain.

23
Q

What are electrolytic lesions?

A

Lesions to the brain caused by induced electrical currents.

24
Q

What are excitotoxic lesions?

A

Lesions caused by chemicals which over-stimulate neurons to death.

25
Q

What did Gale et al (2004), Marren (1999), Nader et al., (2001), and Sananes and Davis, (1992) find about lesions to the amygdala in rats?

A

Lesions to the amygdala impair rats’ pavlovian fear conditioning, regardless of whether the lesions occur before, during or after learning.

26
Q

What did Antoniadis et al., (2007) find about lesions to the amygdala of monkeys?

A

That impairments in Pavlovian fear conditioning were induced, but only if the lesions were made before learning.

27
Q

How can specific brain areas be silenced - how can their activity be decreased or inhibited?

A

Using chemicals:

  • Tetrodotoxin (TTX): which blocks sodium channels, preventing action potentials from firing in the designated brain area.
  • Baclofen and Muscimol, which are agonists for GABA receptors. As GABA receptors inhibit neurons, increasing their activation leads to a functional silencing within target areas.
28
Q

What did Muller et al., (1997) find about the amygdala in rats?

A

That fear memories were significantly impaired when the amygdala was functionally silenced before fear conditioning and before fear testing.

29
Q

What is cellular consolidation?

A

The stabilisation of a memory which requires a multitude of cellular processes.

30
Q

What is the evidence that supports the idea that memory consolidation requires the synthesis of new proteins?

A

There is increased gene expression at learning - suggesting that the proteins being produced as a result of this gene expression are required for consolidation.

31
Q

What does arc stand for and why is it needed?

A

Activity-related cytoskeletal-associated protein is supposedly required for memory consolidation.

32
Q

What did Ploski et al., (2008) find about the need for arc protein?

A

Found that the consolidation of fear memories was impaired when the synthesis of arc protein in the amygdala was inhibited.

33
Q

What did Ploski et al., (2008) find about the regulators of arc expression?

A

The increase in arc expression was dependent on the increase of signalling in the ERK/MAPK pathway.

34
Q

What regulates arc expression and why?

A

The ERK/MAPK pathway involves protein enzymes which phosphorylate enzymes, activating them, subsequently leading to the activation of further downstream components of the pathway.

35
Q

What did Shafe et al (2000) find out about the importance of ERK/MAPK signalling?

A

The inhibition of the ERK/MAPK pathway impairs the consolidation of fear memories in the amygdala.

36
Q

What did Lee and Kim, (1998) and Miserendino, (1990) find about NMDA receptors and fear conditioning?

A

The introduction of an NMDA antagonist blocks the acquisition of fear conditioning. Supposedly because the NMDA receptors could not be activated, so the ERK/MAPK pathway was not activated and therefore the arc protein was not expressed/not enough was produced.

37
Q

What is the NMDA receptor antagonist which is used in a study by Lee and Kim, (1998) and Miserendino, (1990) ?

A

AP-5

38
Q

What did Bauer et al (2002) find about NMDA receptor antagonism?

A

That NMDA receptor antagonism causes impairments in STM as well as LTM, suggesting that NMDA receptors may be involved in the general process of learning/memory acquisition.