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PMCOL 305 > 5 - neuroplasticity > Flashcards

5 - neuroplasticity Flashcards

1
Q

what is neuroplasticity

A

brain’s ability to reorganize and restructure itself

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2
Q

what are 3 main things associated with neuroplasticity / what happens

A

formation/death of neurons
formation/loss of new neuronal connections
strengthening/weakening of existing connections

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3
Q

what do drugs do to memory and why

A

decrease in neurogenesis is linked to memory issues

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4
Q

what are dendritic spines

A

dendritic arms covered in spiny extensions

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5
Q

what can cause dendritic arms to change shape

A

learning, stress, drugs

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6
Q

whats the role of dendritic spines in the nucleus accumbens

A

this is where synaptic contacts are made with other neurons (medium spiny neurons)

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7
Q

where are most dendritic spines

A

where there are lots of glu receptors (responding to various components of reward pathway)
-but they can be in many brain regions

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8
Q

what happens in dendritic spines

A

major site of mostly excitatory input from other neurons, mostly from PFC, also hippocampus and amygdala

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9
Q

what receptor types do dendritic spines have

A

for glutamate

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10
Q

what causes the change and shape and density of dendritic spines (what allows it to do this)

A

actin rearrangement

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11
Q

where are the glu receptors on dendritic spines

A

the tip of projections

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12
Q

what flows through activated glu receptors in dendritic spines

A

calcium

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13
Q

what does calcium flow through activated glu receptors cause

A

actin structure to change

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14
Q

what happens when glu activates their receptor in the dendritic spine

A

calcium pores open to enter, actin changes shape

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15
Q

what do drugs do to the dendritic spine genes

A

modulate genes for the cytoskeleton

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16
Q

what do opiates do to dendrites in the NAc

A

decrease spines and number of dendrites

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17
Q

what do opiates do to dendrites in the VTA

A

decrease cell body size

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18
Q

what do stimulants do to dendritic spines

A

increase growth

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19
Q

what do stimulants do to dendrites in the NAc

A

increase number of dendrites and the density and size of of the spines

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20
Q

what do stimulants do to dendrites in the VTA

A

increase density and size of spines

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21
Q

which part of brain gets increased or decreased number of dendrites due to drugs

A

the NAc

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22
Q

what is thought to cause the basis for experience-dependent learning and memory

A

synaptic plasticity of dendritic spines

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23
Q

what does glu do in memory related processes

A

plays a critical role in mediating memory related processes

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24
Q

where are most of the dendritic spines found

A

on MSN in nucleus accumbens

Also VTA, hippo & amyg

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25
Q

what happens to AMPA and NMDA receptors with cocaine exposure

A

increase AMPA receptor and AMPA:NDMA ratio

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26
Q

what happens when AMPA receptors are activated by glu

A

increase entry of calcium

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27
Q

what is long-term potentiation

A

a persistent strengthening of synapses based on recent patterns of activity
-lasting potentiation of excitatory synaptic transmission

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28
Q

what does increased calcium entry into dendritic spines do

A

trigger structural changes

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29
Q

what is important with long-term potentiation (what is it a hallmark of)

A

learning

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30
Q

what are the types of dendritic spiny DA releasing neurons

A

type 1 is affected by glu (grows more spines)

type 2 not affected

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31
Q

what happens when type 1 DA releasing neurons are exposed to cocaine

A

increase glu receptors

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32
Q

what happens with increase glu receptors (what does this cause)

A

more potential for excitatory input from other neurons

33
Q

what happens when type 2 DA releasing neurons are exposed to cocaine

A

nothing

34
Q

where are these type 1 and type 2 receptors

A

ventral tegmental area (in rats)

35
Q

even with drug use extinction, can you reinstate drug seeking behaviour? how? how fast do you see brain changes?

A

yes, things like flashing a light (if that was associated to drug taking) can elevate AMPA/NMDA ratio within 15 mins

36
Q

what happens when you lesion glu projections from PFC to nucleus accumbens

A

there is no glu signal or input, no drug reinstating behaviours can happen

37
Q

can anticipation affect dendritic spines

A

yes, it can increase the size and stuff

38
Q

what causes over-leaning in dendritic spines

A

strengthening of pathways by glu

39
Q

what stimulates BDNF production

A

calcium influx

40
Q

what do stimulants do to BDNF levels

A

increase, even during abstinence

41
Q

what does high BDNF levels do

A

more spines and increased cell body size

42
Q

what does morphine do to BDNF levels

A

reduce

43
Q

what does low BDNF levels do

A

fewer spines, less AMPA receptors

44
Q

what does BDNF do to ERK

A

affects its pathway

45
Q

what are some main roles of the ERK pathway

A

affect genes that code for cytoskeleton proteins involved in spine formation

46
Q

where is the growth of new neurons essential for psychiatric issues and deciphering between cues that signal pleasant or unpleasant experiences

A

hippocampus

47
Q

what 4 things can inhibit neurogenesis

A

corticosteroids (stress hormones)
anxiety
depression
addiction

48
Q

what 4 things can stimulate neurogenesis

A

enriched environment
exercise
antidepressions
electroconvulsive shock therapy

49
Q

what are the main areas of neuronal growth

A

subventricular zone
olfactory bulb
subgranular layer of the hippocampus dentate gyrus

50
Q

does the subventricular zone alter neurogenesis in response to drugs

A

no

51
Q

does the olfactory bulb alter neurogenesis in response to drugs

A

no

52
Q

does the subgranular layer of the hippocampus dentate gyrus alter neurogenesis in response to drugs

A

yes!

53
Q

what is a lab technique used to measure new neuronal growth

A

brdU (mimics thymidine) that only interact with DNA when replicating, antibody to brdU will produce a signal when cells contiain brdU in their DNA

54
Q

where do progenitor cells arise

A

subgranular zone in the hippocampus

55
Q

what happens in the granular cell layer

A

cells born from the subgranular zone migrate and mature here - establish neuronal connections

56
Q

where is the subgranular zone and the granular cell layer

A

subgranular zone is beneath the granular cell layer

57
Q

what does chronic cocaine do to BrdU incorporation

A

decrease (decreased proliferation)

58
Q

what is proliferation

A

formation of new neurons

59
Q

what does acute cocaine do to BrdU incorporation

A

single exposure has similar results but it recovers after a few days

60
Q

what does binge ecstasy do to brain (neurogenesis)

A

doesnt decrease neurogenesis but kills new neurons

61
Q

what does methamphetamine do to brain (neurogenesis)

A

impairs both proliferatoin and survival

62
Q

what does nicotine do to brain (neurogenesis)

A

impairs neurogenesis and certain types of memory

63
Q

what does lack of sleep do to brain (neurogenesis)

A

decrease neurogenesis

64
Q

what does chronic morphine do to brain (neurogenesis)

A

decrease neurogenesis (so its not the stimulants that do this, its the addictive nature of the drugs)

65
Q

what 4 things are altered when neurogenesis is inhibited (rats, experimentally)

A
  • self-administer more cocaine
  • take higher doses
  • work harder for more doses
  • harder to extinguish behvaiours
66
Q

how are rates of addiction different with animals that have neurogenesis inhibited

A

more vulnerable to addiction

67
Q

how did they inhibit neurogenesis in the experiment

A

X-ray irridation of hippocampus in rats

68
Q

why is it harder to extinguish a behaviour if neurogenesis is inhibited

A

because extinguishing a behaviour is still a type of learning

69
Q

what is contextual memory

A

associating place with events

memories triggered by smells, sights, taste… certain contexts

70
Q

what part of the brain is associated with contextual memory

A

hippocampus (learning and memory centre)

71
Q

what happens with contextual memory learning with drug use (hippocampus)

A

deficits in memory processing of drug-associated cues, enhancement of drug-reinforcement learning

72
Q

how is glutamate affected with a lack of new hippocampus neurons in hippocampus

A

excessive glutamate release from HC onto PFC and NAc neurons in presence of drugs/cues

73
Q

what happens with excessive glutamate release at PFC

A

loss of neuronal mass and dysfunction

74
Q

what happens with excessive glutamate release at NAc

A

excessive stimulation, general dysfunction

75
Q

what are 3 possible mechanisms for impaired neurogenesis

A
  • drugs that activate DA receptors in hippocampus
  • drugs that cause oxidative stress (damage mitochondria in developing neurons)
  • influence levels of growth factors (BDNF, VEGF)
76
Q

is CBD or THC active

A

THC

77
Q

what does CBD do to neurons

A

increase neurogenesis, increase cell survival and maturation

78
Q

what does THC do to neurons

A

reduce learning abilities (in mice) and no effect on neurogenesis

79
Q

where can CB1 receptors be found

A

dentate gyrus

PMCOL 305 (26 decks)

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