Neuroplasticity

neuroplasticity

persistent change in neural output based on a prior experience

f

*t/f* an increase in neural output during the application of a stimulus, which returns to baseline after the stimulus is removed, is an example of neuroplasticity

t

*t/f* a decrease in neural output that begins with the application of a stimulus and persists after the stimulus is removed is an example of neuroplasticity

t

*t/f* an increase in neural output that begins with the application of a stimulus and persists after the stimulus is removed is an example of neuroplasticity

t

*t/f* neuroplasticity often requires repeated episodes of the stimulus/experience

neuroplasticity

__________ is one of the most important concepts for rehabilitation

e

which changes can neuroplasticity cause?
a. output
b. structure
c. connections
d. function
e. any of the above

activity-dependent

2 examples of synaptic -___ neuroplasticity:

1. habituation

2. hippocampal long-term potentiation (LTP)

synaptic

activity-dependent neuroplasticity such as habituation and hippocampal long-term potentiation depend on *physical/synaptic* activity

habituation

decrease in response to a repeated benign stimusus
⇒functionally: "tune things out"
⇒brief vs. long presentation of the stimulus
⇒CNS more aware of changes than continual stimulation

changes

the CNS is more aware of *continual stimulation/changes*

both

habituation occurs with *brief/prolonged/both* presentation of stimulus

short term

decreased neurotransmitter release is a *short term/prolonged* cellular mechanism of habituation

short term

reduced free intracellular calcium is a *short term/prolonged* cellular mechanism of habituation

prolonged

receptor expression/protein synthesis is a *short term/prolonged cellular mechanism of habituation

prolonged

fewer synaptic connections are a *short term/prolonged* cellular mechanism of habituation

presynaptic

*presynaptic/postsynaptic* changes are short-term cellular mechanisms of habituation

postsynaptic

*presynaptic/postsynaptic* changes are prolonged cellular mechanisms of habituation

neurotransmitter

changes in

1. ______________ release

2. postsynaptic response

3. number of synaptic connections can lead to changes in motor output/strength

postsynaptic

changes in

1. neurotransmitter release

2. _____________ response

3. number of synaptic connections can lead to changes in motor output/strength

synaptic

changes in

1. neurotransmitter release

2. postsynaptic response

3. number of __________ connections can lead to changes in motor output/strength

tactile defensiveness

A type of sensory defensiveness in which a child overreacts or avoids touching certain textures.
⇒use concepts of habituation to gradually expose them to gentle and progressively more intense stimuli

vestibular

_____________ disorders can be treated with concepts of habituation by repeating movements that cause dizziness/nausea with a goal of decreasing the response to those stimuli

long term potentiation/LTP

__________ _______ ___________ in the hippocampus:
⇒a possible cellular mechanism for learning and memory
⇒new neurons are very limited - so how do we learn and remember?
⇒not unique to the hippocampus

e

long-term potentiation occurs in the:
a. cortex
b. hippocampus
c. cerebellum
d. amygdala
e. all of the above

f

*t/f* long-term potentiation is unique to the hippocampus

Hebb's postulate

_______'__ __________: *cells that fire together, wire together*
⇒when an axon of cell A is near enough to excite cell B or repeatedly or consistently takes part in firing it, some growth or metabolic changes take place in one or both cells such that A's efficiency, as one of the cells firing B, is increased.

silent

one mechanism of LTP is conversion of __________ synapses
⇒ synapse has NMDA receptors only ⇒ glutamate binds to NMDA receptor⇒ calcium enters ⇒AMPA receptors are recruited ⇒ synapse becomes functional/active

calcium/Ca2+

mechanisms of LTP:
influx of ___________ through NMDA receptors activates downstream signaling pathways and insertion insertion of AMPA receptors into the post-synaptic membrane which allows Na+ influx

NMDA

mechanisms of LTP:
influx of Ca2+ through _______ receptors activates downstream signaling pathways and insertion insertion of AMPA receptors into the post-synaptic membrane which allows Na+ influx

AMPA

mechanisms of LTP:
influx of Ca2+ through NMDA receptors activates downstream signaling pathways and insertion insertion of _________ receptors into the post-synaptic membrane which allows Na+ influx

sodium/Na+

mechanisms of LTP:
influx of Ca2+ through NMDA receptors activates downstream signaling pathways and insertion insertion of AMPA receptors into the post-synaptic membrane which allows _________ influx

a

what can pass through NMDA receptors?
a. calcium and sodium
b. calcium only
c. sodium only

c

what can pass through AMPA receptors?
a. calcium and sodium
b. calcium only
c. sodium only

AMPA

*NMDA/AMPA* receptors are inserted into the post-synaptic membrane as a part of long-term potentiation

fast

insertion of NMDA receptors for long-term potentiation is a relatively *fast/slow* process

slow

structural remodeling is a relatively *fast/slow* process

dendritic spine

structural remodeling involves new __________ _________ formation

structural remodeling

new dendritic spine formation
⇒altered gene expression and transcription activation

gene

structural remodeling
⇒new dendritic spine formation
⇒altered ________ expression and transcription activation

t

*t/f* the mechanism influences the duration in which neuroplasticity lasts

a

which of the following has the *shortest* duration of LTP?
a. downstream signaling, receptor trafficking
b. structural remodeling
c. activation of synapses
d. altered gene expression

b

which of the following has the *longest* duration of LTP?
a. downstream signaling, receptor trafficking
b. structural remodeling
c. activation of synapses
d. altered gene expression

c

which of the following has the *second shortest* duration of LTP?
a. downstream signaling, receptor trafficking
b. structural remodeling
c. activation of synapses
d. altered gene expression

d

which of the following has the *second longest* duration of LTP?
a. downstream signaling, receptor trafficking
b. structural remodeling
c. activation of synapses
d. altered gene expression

associativity

Rule #1 of LTP: _______________, or Hebb's postulate: pre-synapse and post-synapse are activated together

cooperativity

Rule #2 of LTP: _________________: LTP can be induced either by strong tetanic stimulation of a single pathway to a synapse, or cooperatively via the weaker stimulation of many

specificity

Rule #3 of LTP: ____________: LTP at one synapse does not spread to other synapses

f

*t/f* LTP at one synapse can spread to other synapses

c

LTP can be induced by:
a. strong tetanic stimulation of a single pathway to a synapse
b. cooperatively via the weaker stimulation of many
c. a or b

t

*t/f* for neuroplasticity, the change in neural output must outlast the stimulus

rehabilitation

neuroplasticity is a fundamental component of ___________

synaptic

habituation and LTP are __________ activity dependent

decrease

habituation is a(n) *increase/decrease/either* in response to a repeated benign stimulus

learning

hippocampal LTP is a cellular mechanism for ___________ and memory

intermittent

neuroplasticity in the respiratory system:
*intermittent/sustained/both* hypoxia can cause long term facilitation of respiratory motor output
⇒clinical implications for incomplete SCI

serotonin

the mechanism of hypoxia induced plasticity is spinal ______________ receptor activation

neuromodulators

changes in ______________ can influence expression of neuroplasticity
⇒there may be ways to increase the potential of inducing neuroplasticity
⇒spinal stimulation

additive

coupling therapies have a(n) ____________ effect for neuroplasticity

e

neurons are sensitive to which of the following?
a. hypoxia
b. infection
c. chemical
d. mechanical
e. all of the above

CNS

spinal cord injury affects the *CNS/PNS/both*

CNS

stroke affects the *CNS/PNS/both*

CNS

TBI affects the *CNS/PNS/both*

both

demyelination affects the *CNS/PNS/both*

PNS

neuropathy affects the *CNS/PNS/both*

epineurium

surrounds the entire nerve

perineurium

surrounds each fascicle

endoneurium

surrounds each individual axon

neurapraxia

conduction disruption due to focal demyelination (traumatic myelopathy)
ex: carpal tunnel, Saturday night palsy

axonotmesis

demyelination, axonal damage, intact epineurium (traumatic axonopathy)

neurotmesis

demyelination, axonal damage, and severed epineurium (traumatic axonopathy or severance)

mild

neuropraxia is a *mild/moderate/severe* classification of PNS injury

moderate

axonotmesis is a *mild/moderate/severe* classification of PNS injury

severe

neurotmesis is a *mild/moderate/severe* classification of PNS injury

neurapraxia

recovery of ______________ occurs through:

1. removal of pressure

2. reinstatement of blood flow

3. remyelination over a period of days/weeks/months

proximal

for axonotmesis and neurotmesis, the *proximal/distal* segment of an axonal injury is connected to the cell bodies

die

for axonotmesis and neurotmesis, the closer the injury is to the cell soma, motor point, sensory receptor = greater likelihood the cell will *survive/die*

survive

axonotmesis and neurotmesis beyond 15% of the axon's distance from the cell body = cell will *survive/die*

15

a cell will survive if the axonotmesis/neurotmesis is beyond ____% of the axon's distance from the cell body

a

degeneration affects the:
a. axon
b. cell body
c. cell body and axon
d. only distal segment of axon
e. only proximal segment of axon

a

axon retraction affects the:
a. axon (both segments)
b. cell body
c. cell body and axon
d. only distal segment of axon
e. only proximal segment of axon

b

central chromatolysis affects the:
a. axon
b. cell body
c. cell body and axon
d. only distal segment of axon
e. only proximal segment of axon

c

edema affects the:
a. axon
b. cell body
c. cell body and axon
d. only distal segment of axon
e. only proximal segment of axon

a

sprouting affects the:
a. axon
b. cell body
c. cell body and axon

e

retrograde degeneration will affect the:
a. axon
b. cell body
c. cell body and axon
d. only distal segment of axon
e. only proximal segment of axon

retrograde

____________ degeneration: proximal segment; similar to degeneration of distal segment but only 1 or 2 nodes of ranvier because it is still getting nourishment from the cell body

slower

degeneration in the CNS is the same as PNS but *faster/slower*

PNS

functional regeneration occurs in the *CNS/PNS/neither/both*

CNS

very little (if any) regeneration occurs in the *CNS/PNS/neither/both*

permissive

the PNS has a *permissive/inhospitable* environment for regeneration

inhospitable

the CNS has a *permissive/inhospitable* environment for regeneration

1-2

regeneration in the CNS is slow and limited, ~___-___mm/day

rehabilitation

___________ will *encourage* plasticity in the spinal cord and brain

b

how long does it take for proximal axons in proximal stump to sprout after a clean cut injury?
a. a few minutes
b. a few hours
c. a day or 2
d. 1 week

d

how long does it take for proximal axons in proximal stump to sprout after a crush or tear injury?
a. a few minutes
b. a few hours
c. a day or 2
d. 1 week

clean cut

a *tear/clean cut/crush* injury will likely have sprouting more quickly

sprouts

growth ______________ (tips called growth cones) search for schwnn cells in endoneurial tube of distal stump

growth cone

the tip of a growth sprout is called a __________ __________

schwann cells

growth sprouts search for _________ ________ in the endoneurial tube of the distal stump

endoneurial tube

growth sprouts search for schwann cells in the ____________ ____________ of the distal stump