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mental health + neurobiology > neuronal plasticity > Flashcards

neuronal plasticity Flashcards

1
Q

memory

A

simply describes stored information about past (recent or distant) experiences

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2
Q

what are 3 main types of memory

A

1.Sensory
2.Working
3.Long-term

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3
Q

2 categories of long term memory

A

1.declarative memory
2.procedural memory

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4
Q

what is declarative memory

A

memory that can be expressed in language – facts or information that have been learnt

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5
Q

what is procedural memory

A

are ones that involve the learning of skills – riding a bicycle, playing a musical instrument

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6
Q

what are 2 things declarative memory are divided into?

A

1.semantic memory
2.episodic memory

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7
Q

semantic memory

A

which is material learnt independent of its context. An example would be knowing the names of colors.

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8
Q

Episodic memory

A

particular context, such as memory of a particular event

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9
Q

in memory what is explicit

A

where information is consciously held and actively fed into long-term memory storage

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10
Q

in memory what is implicit

A

where information is integrated into long-term memory without our conscious recollection

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11
Q

why is memory important?

A

provides a template/framework for your responses to different situations

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12
Q

the limbic system

A

hippocampus is involved in many forms of memory but particularly spatial and long-term explicit memory

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13
Q

the limbic system-amygdala

A

link to negative emotional memory, learned fear.

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14
Q

the pre-frontal cortex

A

plays a key role in working memory and integration of information for transfer to long-term memory

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15
Q

the striatum

A

plays a key role in learning of skills and habits (this also links to it’s role in the control of movement and procedural learning)

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16
Q

the cerebellum

A

plays a key role in procedural learning

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17
Q

neocortex

A

developmentally newer regions of the cortex that have all six layers of cells present
-includes most of the prefrontal cortex and also the cortical association areas in the temporal and parietal regions

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18
Q

engram

A

describe the ‘memory trace,’ that allows a memory to be stored

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19
Q

what are the 2 ways memory is stored in engram?

A

1.electrically
2.physically

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20
Q

what is the electrical way in engram

A

as a pattern of activity within neuronal circuits

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21
Q

what is the physical way in engram

A

through changes in the cellular make-up, this could be morphological or metabolic/functional

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22
Q

what 3 locations can memory be located at?

A

1.The engram
2.The engram cell
3.the engram circuit

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23
Q

The engram(location)

A

resulting from subcellular changes

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24
Q

The engram cell

A

changes at the single neuron level

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25
Q

engram circuit

A

seen as changes at a network level

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26
Q

papez ciruit

A

the cyclical circuitry

27
Q

what happens in papez circuit?

A

1.electrical activity passes from hippocampus through limbic system
2.then back to the limbic system
3.this type of activity holds information in working memory
4.can also contribute to emotional processing

28
Q

Neuroplasticity

A

describes the ability for a neuron or neuronal network to alter its activity, to increase/decrease it’s response to certain stimuli or inpu

29
Q

what 4 routes can occur in neuroplasticity?

A

1.rewiring
2.reconnecting
3.retracting
4.regenerating

30
Q

rewiring

A

changing activity at the level of the single neuron

31
Q

Reconnecting

A

changing the connectivity of neurons

32
Q

Retracting

A

pruning connections to streamline activity

33
Q

Regenerating

A

growth of new neurons (neogenesis)

34
Q

what do the 4rs lead to?

A

enhancement of reduction in the likelihood of a particular neuron and/circuit being activated

35
Q

what 2 modals are in the 4rs?

A

1.Long-term potentiation
2.Long-term depression

36
Q

long term potentiation(Tim Bliss and Tereje Lamo 1973)

A

1.they found that when they recorded in the hippocampus (a key area for learning and memory) of rabbits
2.if they applied a brief period of high frequency stimuli and then went back to the regular stimulation levels
3.activity in the stimulated population of neurons was increased
4.increase lasted for hours!

37
Q

how did the induction of rapid onset occur

A

LTP was dependent on activation of the NMDA

38
Q

NMDA

A

glutamate receptor

39
Q

what is NMDA dependent on?

A

voltage dependent due to the channel being blocked by magnesium (Mg2+), this block is removed by the high frequency stimulation and this allows the channel to open.

40
Q

what do NMDA channels allow?

A

allow entry of Ca2+ into the post synaptic terminal, and this calcium entry triggers second messenger cascades that can induce plastic changes within the cell

41
Q

2 what plastic changes are made in NDMA channels

A

1.structural (e.g. changing the synapse shape)
2.functional (e.g. changing receptor sensitivity or number)

42
Q

what changes occur in NDMA channels?

A

pre-synaptically that leads to an increase in transmitter release. Overall this leads to an increased response to later stimulation

42
Q

what happens when there is increased response to later stimulation in NDMA channels

A

NMDA-receptor dependent LTP

43
Q

what can NMDA-receptor dependent LTP be induced by?

A

metabotropic glutamate receptors

44
Q

long term depression

A

model that would allow information to be deleted from the circuitry
-is induced by low level activation of the receptors.

45
Q

what 2 forms does long term depression have ?

A

1.NMDA- dependent
2.Non-NMDA dependent

46
Q

how can In-vitro LTD be induced?

A

low frequency stimulation (1Hz) for an extended period of time (15 mins)

47
Q

what does in-vitro cause ?

A

causes enough depolarisation to open some NMDA receptors, but not enough to activate LTP

48
Q

what happens when there is depolarisation of NMDA receptors but not enough to activate LTP?

A

leads to low-level calcium entry a reduced level of activation of the second messenger cascades, internalisation of the AMPA receptors from the post-synaptic membrane and retraction of spine morphology

49
Q

what happens after retraction of spine morphology?

A

Pre-synaptically, this results in decreased transmitter release. All of these reduce the likelihood of the neuron firing again.

50
Q

depotentiation

A

possible to reset LTP using LTD

51
Q

what does LDT play a role in?

A

thought to play a role in procedural/skills learning, and also in conditioned learning (such as fear conditioning), where improved performance and responsiveness is dependant on removing errors

52
Q

what happens during induction of LTP and LTD

A

range of second messenger cascades are activated.

53
Q

what do NMDA receptors activation allow?

A

allows Ca2+ entry, which triggers intracelllular signalling cascades.

54
Q

Type 1 mGluR

A

metabotropic glutamate receptors) activates PLC (phospholipase C) which can trigger many kinase cascades activating genes that increase protein synthesis

55
Q

what else do type 1 mGlurR activate?

A

trigger Ca2+ release from intracellular stores

56
Q

Type 2 mGLuR

A

modulate cAMP levels.

57
Q

what can activation of cascades in MGLuR lead to?

A

upregulation of receptors, with new AMPA receptors being inserted into the membrane, which increases the amount of depolarisation when the next stimulus arrives.

58
Q

what do metabotropic glutamate receptor change?

A

shape of the synapse or the number of synapses linked to the potentiated synapse, increasing the surface area of the connection, increasing the likelihood of transmission.

59
Q

synaptic pruning

A

reduction in spines (the points of connection, where the synapses are located

60
Q

memory loss

A

associated with cognitive decline associated with dementia, or as a result of stroke or traumatic brain injury.

61
Q

2 main forms of amnesia

A

1.anterograde
2.retrograde

62
Q

anterograde

A

loss of memory of events following the trauma

mental health + neurobiology (45 decks)

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