Learning and Memory Flashcards

1
Q

Learning

A

Acquisition of new information or knowledge

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1
Q

Memory

A

Storage or retention of acquired knowledge

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2
Q

Engram - definition

A

Physical representation or location of memory

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3
Q

Cortexes involved with memory

A

Temporal, parietal, olfactory and prefrontal

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4
Q

Brain areas concerned with declarative memory

A

Hippocampus
Parahippocampal cortex

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5
Q

Brain areas concerned with emotional memory

A

Amygdala
Hypothalamus

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6
Q

Brain areas concerned with procedural memory

A

Cerebellum stores movement-based memory
Brainstem
Striatum

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7
Q

Declarative memories

A

Things you think about
Episodic
Somatic

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8
Q

Emotional memory

A

Preferences and aversions

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9
Q

Procedural memory

A

Motor skills
Associations
Priming cues
Puzzle solving

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10
Q

HM

A

Had his temporal lobes removed to treat epilepsy
Could not form new explicit memories, but long term procedural was intact
Severe anterograde amnesia

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11
Q

Hebb’s law

A

When two neurones are active together then that synapse will become stronger.
Synapses strengthened by intense activity
Memory depends on populations of interacting neurons
Pattern of strengthened synapses defines memory

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12
Q

Engram

A

The pattern of closely connected neurons that forms a physical memory

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13
Q

How do we study synaptic strengthening?

A

The recording of the membrane potential of neurons

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14
Q

How does a synapse get stronger?

A

If there are a lot of action potentials in a short time, there is a potentiated AMPAr EPSP
This causes the strengthening of the synapse and can last forever

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15
Q

What is EPSP

A

Excitatory Post-Synaptic Potential

16
Q

What is the increase in strength after repeated stimulation called?

A

Long Term Population (LTP)

17
Q

Dual gating of NMDA receptor

A

Have a magnesium block, so can only fire when the cell is depolarised.
Glutamate must bind as well.
Both Ca and Na can then flow through the NMDAr channel

18
Q

NMDA and memory

A

Depolarisation to repetitive activation of AMPAr relieves Mg2+ block
Both Ca and Na flow through NMDAr channel
Ca-entry causes cellular changes that lead to increased AMPAr response – LTP

19
Q

How is LTP manifested Postsynaptically?

A

More AMPAr
More sensitive AMPAr
More synapses

20
Q

How is LTP manifested presynaptically?

A

Increased release
More release sites
More vesicles

21
Q

LTP induction mechanisms

A
  • Burst of activity releases glutamate and activates NMDA
  • Phosphorylation of AMPAr by PKC
  • Insertion of new receptors by CaMKII.
  • Synthesis of new receptors
  • Retrograde messenger – such as nitric oxide - presynaptic changes
  • Synthesis of new AMPA receptors and exchange of AMPA receptor subunits
22
Q

Phosphorylation of AMPAr by PKC

A

PKC here but also other kinases are involved
This phosphorylation is what leads to hypersensitive AMPA receptors

23
Q

NMDAr antagonists will _ learning

A

Inhibit

24
Q

Composition of a memory

A

It is in fact made up of several different types of memory
These can include association and priming cues.

25
Q

Classical conditioning and memory

A

Triggers
This links to addiction and craving due to association

26
Q

Reactivating a memory _ it

A

Strengthens

27
Q

Examples of cognition enhancers

A
  • Cholinergic modulation: anticholinesterases - donepezil (Aricept), galantamine or agonists - nicotine, arecoline
  • Stimulants - amphetamine, methylphenidate, modafanil, caffeine
  • 5HT drugs – particularly 5HT6 antagonists
  • GABAA receptor blockers - inverse agonists – suritozole
  • AMPAkines - positive AMPAr modulators - piracetam, IDRA-21
  • mGluR drugs – particularly mGluR5 positive allosteric modulators
28
Q

Causes of amnesia

A

Drug induced such as alcohol
Head trauma - temporary or permanent

29
Q

Retrograde amnesia

A

Retrograde is a struggle to recall preexisting memories

30
Q

Anterograde amnesia

A

Anterograde is the inability to form new memories

31
Q

Dementias

A
  • Loss of multiple memory categories
  • Inability to form new memories (learning)
  • Associated with general cognitive decline
  • Memory impairment first presenting symptom