Chapter 7 Neuroplasticity Flashcards

1
Q

what is habituation

A

decrease in a response to repeated, benign stimulus

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2
Q

process of habituation

A

one neuron will release less NT turning down the signaling of that pathway

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3
Q

one of two ways that signaling can be turned down

A

first way: more presynaptic inhibition

two: less presynaptic facilitation (reduce the number of NT that spills out)

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4
Q

what happens if the brain feels better?

A

that pathway may not be turned on as much

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5
Q

habituation is short term or long term

A

short term

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6
Q

post synaptic terminal can take receptors away. this is…

A

long term

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7
Q

tactile defensiveness

A

turn down NT release, repetitively doing it then a remodeling of post synaptic membrane

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8
Q

roller coaster and inner ear

A

repetitively on a roller coaster, the inner ear loses NT

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9
Q

Long Term potentiation (LTP)

A

make something easier and in this case it’s easier synaptic signaling

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10
Q

LTP turns up or turns down the strength of synaptic connection

A

turns up the strength

this is easier to signal. process we used everyday to commit something to memory

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11
Q

LTP converts….

A

FROM silent synapses

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12
Q

LTP goes from a _____ synapse to ______

A

silent to active

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13
Q

what is a silent synapse

A

a physical synapse but there is no signal

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14
Q

what are the type of receptors associated with LTP and what do they bind

A

AMPA receptors bind glutamate. this will create AP receptors

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15
Q

receptors of action are located….

A

buried in the cell

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16
Q

NMDA is responsive to

A

glutamate

in our brain the NMDA receptors let in calcium to remodel the cell not an AP

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17
Q

look over slide 10 and in the book

18
Q

process of LTP step one

A

NMDA receptors are activated and calcium tells NMDA receptors to pop up into membrane

19
Q

process of LTP step two

A

glutamate is released to put receptors up into the membrane

20
Q

how does the post synaptic membrane break?

A

breaks into spines which results in spatial summation

depolarizes at each spine. calcium turns on intracellular enzymes that remodel post synaptic membranes and we can get spatial summation

21
Q

Why does the effort of activity go way down?

A

receptors of action goes way down because we not only have receptors of AP but it takes way less effort

22
Q

what is the importance of astrocytes?

A

store and release calcium (cell remodeling)

sotre and release glutamate (release of NT)

23
Q

Long term depression (LTD)

A

turns down strength of signal. LONG TERM

24
Q

LTD converts……

A

to silent synapses

25
LTD tries to do what
repeatedly try to apply benign stimulus | not as many receptors are needed so pulls them away
26
what is excitotoxicity?
when cells are killed, their guts of glutamate are spilled and the glutamate goes to surrounding cells.
27
What does glutamate done after being spilled?
opens NMDA channels on all surrounding neurons and keep them open. this results in TOO much calcium getting in
28
results of too much calcium
glycolysis--> lactic acid--> lower pH turns on protease (eats protein): cell disassembles its own membrane ad protein enzymes are turned on inappropriately and produce free radicals as poison where solute goes, H2O follows=swelling
29
free radicals
stop normal cell processes
30
goals in stroke and head trauma
stroke: restore blood flow head trauma: reduce swelling
31
what is an axonal injury?
an axon is broken
32
3 ways an axon can be broken
1. axon distal will degenerate 2. myelin will degenerate ( these two are direct) 3. muscle will atrophy (indirect)
33
distal degeneration is also called
Wallerian degeneration
34
what piece can regrow?
proximal piece
35
Axonal injury in periphery, 2 ways the target gets a new nerve supply
1. collateral sprouting: surviving axons can send out extra sprouts to innervate what has lost its innervation 2. regenerative sprouting: surviving proximal axon can regenerate itself (this occurs when the cell body survives, 1 inch a month)
36
ways the synapse changes following injury
recovery of synaptic effectiveness, denervation hypersensitivity, synaptic hypereffectiveness, unmasking of silent synapeses, and functional reorganization of cerebral cortex
37
recovery of synaptic effectiveness
neural inflammation squeezes the axon until it shuts off, no AP due to synaptic transmission when the edema is controlled, the axon wakes back up and starts functioning again reduction of swelling in the brain promotes recovery in the brain
38
denervation hypersensitivity
loss of nerve cell produces a hypersensitive presynaptic cell. all are searching for input receptors may be turned on improperly
39
synaptic hypereffectiveness
each terminal bunch makes connection to this downstream axon some sort of damage has taken away the two bottom branches, axon survived proximally and distally but number of connections was reduced body makes connections stronger than they used to be NO spatial summation but overwhelm it with a ton of NT and try to promote an AP
40
unmasking of silent synapses
many silent synapses in the membrane our goal is to wake up silent synapses within the context of meaningful function in the picture blue is NMDA channel, glutamate opens and more go to it
41
functional reorganization of cerebral cortex
synapse that is chosen stops working, wake up other silent synapses to give a route for that message