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PSC3008 > lecture 23 - anya hurlbert > Flashcards

lecture 23 - anya hurlbert Flashcards

1
Q

types of memory:
declarative memories

A
  • facts and events
  • accessible to consciousness
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2
Q

procedural memories:

A
  • skills and behaviours (riding a bike)
  • involves learning a motor response in association with sensory input
  • inaccessible to consciousness, but never forgotten
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3
Q

declarative memory is in what part of the brain

A

medial temporal lobe

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4
Q

working memory is a form of short term memory

A

memory to which you put items that you’re going to do something with
(e.g if you need to remember a number)

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5
Q

long term memory has…

A

greater capacity and is more permanent
(e.g childhood address)

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6
Q

what is consolidation

A

when an item is important enough to continue to remember for a long time it is put into LTM

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7
Q

types of memory loss (amnesia)

A

retrograde and anterograde

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8
Q

retrograde

A

loss of memories from the time before the trauma occurred which disrupted the memory systems (head injury, stroke)

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9
Q

anterograde

A

unable to form new memories but remembers things from before the time of the trauma

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10
Q

can have anterograde and retrograde amnesia due to..

A

extreme drug use
emotional upset
alcoholic blackout

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11
Q

patient HM
- bicycle accident, age 9
- caused epilepsy due to scar tissue which increased severity
- bilateral temporal lobectomy, age 27 (removed part of brain that had the scar tissue)
- he then had partial retrograde amnesia and severe anterograde amnesia
- normal STM
- normal procedural memory

A

he was taught how to do mirror writing at a good level but had no recollection of being taught that but when he tries to do it he did it perfectly

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12
Q

inside the temporal lobe is the…

A

hippocampus

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13
Q

at the foot of the hippocampus is the

A

amygdala

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14
Q

surrounding the hippocampus is areas of the cortex in the

A

temporal lobe

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15
Q

above the hippocampus is part of the thalamus called the

A

mammillary body

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16
Q

how does the cortex lead into the hippocampus

A

cortex –> parahippocampal cortex –> perirhinal cortex –> entorhinal cortex –> hippocampus

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17
Q

those areas together are called

A

rhinal cortex

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18
Q

information comes in (e.g image of a face) and it goes to the visual cortex
from the visual cortex it goes to…

A

cortical association areas

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19
Q

from the cortical association areas it goes through the…

A

rhinal cortical areas then to the hippocampus

20
Q

from the hippocampus, the signal flow out via a cable called the..

A

fornix to the thalamus and hypothalamus which are central to the limbic system (the system of brain areas that are responsible for capturing our emotional responses to stimuli)

21
Q

all these areas together are part of the…

A

medial temporal lobe

22
Q

synaptic plasticity in the hippocampus:
main model for synaptic changes is LTP (long term potentiation) which is…

A

a change in the efficiency of synaptic transmission along a neural pathway, which makes signals travel more readily along that pathway

23
Q

hippocampus neural circuitry:
the perforant pathway comes in from the…

A

entorhinal cortex

24
Q

the axons from the perforant pathway synapse onto the…

A

dentate gyrus cells

25
Q

the dentate gyrus cells have axons that from bundles called the…

A

mossy fibre

26
Q

the mossy fibres then make synapses onto…

A

pyramidal cells in the CA3 segment

27
Q

the CA3 pyramidal cells send axons to make synapses with the…

A

CA1 pyramidal cells (Ca3 to Ca1 is called the schaffer collateral pathway)

28
Q

CA3 neurons send another branch out to the..

A

limbic system

29
Q

CA1 cells send branches back to the entorhinal cortex which then go back out to the..

A

limbic system

30
Q

LTP has been studies specifically at what synapse

A

between the CA3 and CA1 cells

31
Q

early LTP results from a single train of stimuli to the CA3 axons
the CA1 cell will be potentiated and its response to further incoming stimuli will be enhanced

A

late LTP occurs after multiple trains of stimuli
and then a further stimulus that comes into the CA1 cell will be potentiated for much longer

32
Q

LTP is input specific meaning

A

only potentiates response to subsequent stimulus from the same input to the same cell

33
Q

definition of LTP

A

long lasting strengthening of specific synapse

34
Q

requirements of LTP

A
  • strong postsynaptic depolarisation (called cooperativity when achieved by coincidence of multiple inputs)
  • simultaneous pre and post synaptic activity, yielding synapse specificity (called associativity, when weak stimulus gets associated with strong stimulus)
35
Q

consequences of LTP

A

post synaptic response to normal input at that specific synapse is now enhances (i.e EPSP is greater than baseline)

36
Q

strong depolarisation of postsynaptic (CA1) cell may be induced by…

A
  • brief tetanus (high frequency burst) in one input to CA1 cells
  • summation of EPSPs in response to train of stimuli
  • cooperative inputs from multiple afferents (cooperativity)
37
Q

Hebb’s rule

A

“when an axon of cell A excites cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells so that A’s efficiency as one of the cells firing B is increased”

38
Q

summarised to…

A

neurones that fire together wire together

39
Q

forming of associations:
Hebbian synapses

A

neurone in the hippocampus that receives inputs from visual and olfactory cortex
and every time you see the rose you smell the rose, this neurone receives excitation from the visual stimulus and olfactory stimulus and those two stimuli together cause a depolarisation in the neurone strong enough to potentiate further inputs from either set of axons
so now if you only see the rose you can also evoke the smell of it and vice versa as the two inputs have been associated

40
Q

molecular mechanisms underlying LTP
(weak depolarisation)

A

glutamate release form the CA3 neurone onto the CA1 neurone
CA1 has two types of types of glutamate receptors in its membrane (AMPA and NMDA)
AMPA receptor is ligand gated (glutamate binds –> ion channel opens –> Na+ influx)
NMDA receptor is ligand gated and voltage gated. if post synaptic neuron is only weakly depolarised, NMDA receptor remains blocked by Mg ion

41
Q

strong depolarisation

A

when the post synaptic neuron is strongly depolarised, Mg ion is dislodged –> NMDA ion channel opens –> calcium influx

42
Q

strong depolarisation can be caused by…

A

train of impulses or simultaneous activity of multiple inputs which are then associated

43
Q

long term storage (late LTP) requires…

A

new protein and RNA synthesis

44
Q

early LTP is very much like short term sensitisation in aplysia

A

glutamate released from the CA3 cell onto the CA1 cell
binding to the AMPA receptor which allows an influx of sodium which depolarises the postsynaptic membrane
when the NMDA receptor is activated calcium flows through and this happens only if there’s glutamate binding to the NMDA receptors and glycine binding to one part of the NMDA subunit and then very strong depolarisation which pops the Mg out and allows calcium to flow in
this activates protein kinases which sends a retrograde messenger to the CA3 neurone which is though to be NO which increases transmitter release
theres also enhanced efficiency of the AMPA neurones which is caused by phosphorylation

45
Q

late LTP is much like long term sensitisation and classical conditioning in aplysia

A

repeated trains of stimuli increase calcium influx
causes recruitment of adenylyl cyclase,
migration of cAMP kinase to the nucleus,
phosphorylation of CREBs
changes which lead to protein synthesis which then leads to structural changes in the synapse

46
Q

what is long term depression

A

weakening of synapses
removal of unwanted memories

47
Q

LTD at CA3 –> CA1 synapse

A
  • induced by brief low frequency burst in one input to CA1 cell
  • input specific: depresses response to subsequent stimulus from same input to same cell
  • acts by inducing low concentrations of calcium causing weak membrane depolarisation, which causes modest and prolonged elevation of calcium through NMDA receptor channels
  • activation of protein phosphatases
  • decreased efficiency and reduction in number of AMPA receptor channels

PSC3008 (28 decks)

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