Chapter 7 Neuroplasticity Flashcards
what is habituation
decrease in a response to repeated, benign stimulus
process of habituation
one neuron will release less NT turning down the signaling of that pathway
one of two ways that signaling can be turned down
first way: more presynaptic inhibition
two: less presynaptic facilitation (reduce the number of NT that spills out)
what happens if the brain feels better?
that pathway may not be turned on as much
habituation is short term or long term
short term
post synaptic terminal can take receptors away. this is…
long term
tactile defensiveness
turn down NT release, repetitively doing it then a remodeling of post synaptic membrane
roller coaster and inner ear
repetitively on a roller coaster, the inner ear loses NT
Long Term potentiation (LTP)
make something easier and in this case it’s easier synaptic signaling
LTP turns up or turns down the strength of synaptic connection
turns up the strength
this is easier to signal. process we used everyday to commit something to memory
LTP converts….
FROM silent synapses
LTP goes from a _____ synapse to ______
silent to active
what is a silent synapse
a physical synapse but there is no signal
what are the type of receptors associated with LTP and what do they bind
AMPA receptors bind glutamate. this will create AP receptors
receptors of action are located….
buried in the cell
NMDA is responsive to
glutamate
in our brain the NMDA receptors let in calcium to remodel the cell not an AP
look over slide 10 and in the book
okay cool
process of LTP step one
NMDA receptors are activated and calcium tells NMDA receptors to pop up into membrane
process of LTP step two
glutamate is released to put receptors up into the membrane
how does the post synaptic membrane break?
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
Why does the effort of activity go way down?
receptors of action goes way down because we not only have receptors of AP but it takes way less effort
what is the importance of astrocytes?
store and release calcium (cell remodeling)
sotre and release glutamate (release of NT)
Long term depression (LTD)
turns down strength of signal. LONG TERM
LTD converts……
to silent synapses
LTD tries to do what
repeatedly try to apply benign stimulus
not as many receptors are needed so pulls them away
what is excitotoxicity?
when cells are killed, their guts of glutamate are spilled and the glutamate goes to surrounding cells.
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
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
free radicals
stop normal cell processes
goals in stroke and head trauma
stroke: restore blood flow
head trauma: reduce swelling
what is an axonal injury?
an axon is broken
3 ways an axon can be broken
- axon distal will degenerate
- myelin will degenerate ( these two are direct)
- muscle will atrophy (indirect)
distal degeneration is also called
Wallerian degeneration
what piece can regrow?
proximal piece
Axonal injury in periphery, 2 ways the target gets a new nerve supply
- collateral sprouting: surviving axons can send out extra sprouts to innervate what has lost its innervation
- regenerative sprouting: surviving proximal axon can regenerate itself (this occurs when the cell body survives, 1 inch a month)
ways the synapse changes following injury
recovery of synaptic effectiveness, denervation hypersensitivity, synaptic hypereffectiveness, unmasking of silent synapeses, and functional reorganization of cerebral cortex
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
denervation hypersensitivity
loss of nerve cell produces a hypersensitive presynaptic cell. all are searching for input
receptors may be turned on improperly
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
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
functional reorganization of cerebral cortex
synapse that is chosen stops working, wake up other silent synapses to give a route for that message
