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PT 9111 > Synaptic Transmission > Flashcards

Synaptic Transmission Flashcards

1
Q

AP are __ or ___

A

all or none, AP’s are always the same size

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2
Q

AP frequency is linearly correlated with what

A

stimulus intensity and depolarization
more frequent = more intense AP down the axon

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3
Q

how does lidocaine affect action potentials

A

prevents APs by binding to NA channels to impede the transmission of pain (numbing agent that blocks pain)

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4
Q

what types of neurons are unmyelinated and small in diameter
what types of neurons are myelinated and large in diameter

A

unmyelinated/small: type IV motor, type C sensory (slower)
myelinated/large: type 1 or A alpha (faster)

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5
Q

nerve fibres can be categorized according to what two things
what are the two classification systems

A

fibre diameter and conduction velocity
1. based on conduction velocities of different types of motor and sensory nerve fibres
2. for sensory nerve fibres only and is based on diameter and sensory receptors they innervate

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6
Q

which nerve fibre classification is unmyelinated
are these nerve fibres large or small in diameter
these fibres play a role in what type of pain

A

c fibres, small in diameter
slowest when it comes to conduction velocity
diffuse and slow pain

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7
Q

in what ways do nerve fibre types differ

A

respond to treatment/medication differently
differ in stimulus intensity required to activate them

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8
Q

which fibres are fastest and play a role in motor and sensory functions
why are they the fastest

A

A alpha (motor) and A beta (sensory)
they have the thickest diameter and are myelinated

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9
Q

which fibres type is the easiest to activate and require the least amount of stimulus to fire
which fibre type requires moderate input to activate
which fibres require a lot of input to activate

A

A alpha and A beta
A delta
C fibres

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10
Q

name the origination and number of the sensory nerve fibres:
1. A alpha
2. A alpha
3. A beta
4. A delta
5. dorsal root C

A

muscle spindle, annulospiral ending, 1A (largest diameter)
GTO, 1B (largest)
muscle spindle, 2
pain and cold receptors, 3
pain, temperature and other receptors, 4 (smallest)

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11
Q

what does electromyography measure and what does it evaluate

A

measures electrical activity in response to a nerves stimulation of the muscle
evaluates how well and how fast conduction is occurring in specific nerves (measures compound AP or sum of AP of a given fibre)

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12
Q

what is EMG used to assess and what does it assist in telling you

A

neuromuscular abnormalities
assists with localization but doesn’t identify cause

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13
Q

what is the typical response and abnormal response of the muscle when the needle is inserted in an EMG study

A

typical: brief burst of activity
abnormal: twitch or fibrillation

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14
Q

why should EMG be used in conjunction with a clinical assessment

A

because it can lead to misdiagnosis
it is normal for some people to have an absence of a sensory response or fibrillation which may be mistaken for indication of neuropathy

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15
Q

what are the two types of response that can occur at the post synaptic terminal

A

inhibitory (negative change) or excitatory (positive change)

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16
Q

which types of synapses are excitatory
synapses can be either excitatory or inhibitory between ___

A

neuromuscular and neuroglandular
neurons

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17
Q

where are excitatory (EPSP) and inhibitory (IPSP) localized
whether or not an EPSP or IPSP occurs depends on what

A

EPSP: dendritic tree or the soma
IPSP: near or on the soma
the type of receptors that are there

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18
Q

what are graded responses
where does summation occur

A

the adding and subtracting by EPSP (adding) and IPSP (subtracting) until threshold to send an AP is reached
inside the cell

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19
Q

EPSP and IPSP can summate either spatially or temporally, explain what each is

A

spatial: summation due to the release of NT from multiple presynaptic neurons
temporal: frequency at which the synapses are activated over time

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20
Q

compare and contrast ionotropic and metabotropic receptors

A

ionotropic: linked directly to ion channels, immediate effects on post synaptic potential
metabotropic: affects ion channels through intermediates, G protein coupled receptors, slow response following activation

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21
Q

what are the two types of receptors acetylcholine can bind to, say whether they are excitatory/inhibitory or ionotropic/metabotropic

A

nicotinic: excitatory, ionotropic
muscarinic: inhibitory, metabotropic

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22
Q

when there are issues with ACh in the basal forebrain and brainstem, there is an effect on what brain functions
what disease would cause impacts on these brain functions
what is the etiology of this disease

A

learning, memory, arousal and attention
alzheimers disease
plaques and tangles form in the nerves that result in it no longer being functional

23
Q

where in the body is acetylcholine found and which enzyme breaks it down

A

in the CNS (basal forebrain and brainstem) and the PNS (skeletal NMJ)
autonomic NS (pre and post ganglionic (para)sympathetic neurons)
acetylcholinesterase breaks down acetylcholine at the synaptic cleft

24
Q

medication that inhibits which enzyme is used to treat Alzheimer’s disease

A

acetylcholinesterase

25
Q

how do glial cells and glutamate interact
which types of receptors does glutamate bind to
glutamate makes up a majority of the ___ neurons in the ___

A

glial cells release and take up glutamate
ionotropic and metabotropic
excitatory, CNS

26
Q

why are elevated levels of glutamate neurotoxic
explain how this occurs with neural injury

A

because glutamate initiates a cascade of cell death
when there is injury to the brain the cellular processes in that area stop, one of the processes that stops is the uptake of glutamate out of the cleft so glutamate levels become elevated

27
Q

which neurotransmitter plays a key role in synaptic plasticity

A

glutamate

28
Q

explain the role of GABA (inhibitory/excitatory?, ionotropic/metabotropic?)
GABA is common to ___

A

is the major inhibitory NT
has both ionotropic and metabotropic receptors
common to interneurons

29
Q

what is gamma hydroxybutyrate (GHB)?

A

a naturally occurring NT and precursor to GABA, glutamate and glycine
is also a CNS depressant (used as a date rape drug)

30
Q

how are dopamine levels different in individuals with Parkinson’s disease and psychiatric disorders
in what brain regions is dopamine implicated in

A

lower dopamine levels, meds containing dopamine can alleviate symptoms
implicated in many brain regions (corpus striatum, substantia nigra)

31
Q

where is norepinephrine produced in the CNS and what does NE act as
what activities does NE influence

A

in the locus coeruleus (in pons)
acts as a NT and stress hormone in the CNS and PNS
sleep (low levels) / wakefulness (high levels), attention, feeding behaviour

32
Q

what structure releases NE in the PNS
which drugs block the effects of NE

A

sympathetic ganglia
alpha and beta blockers because they bind to NE receptors

33
Q

where are neuropeptides produced and what do they mediate

A

in the cell soma with no synthesis at terminals
mediators of inflammation and tissue repair

34
Q

what types of nerve fibres do neuropeptides have
neuropeptides have ___ and more ___ action and can be ___ or ___
neuropeptides are active in both the ___ and ____

A

sympathetic and cholinergic
slower, prolonged, excitatory, inhibitory
CNS and pNS

35
Q

what is substance p
where is substance p synthesized and what actions does it have

A

a neuropeptide
dorsal root ganglia
vasodilation, increased vascular permeability, protein extravasation after injury (proteins move from blood to tissues to stimulate cell growth)
stimulates proliferation of epithelial, vascular and connective tissue

36
Q

what is anterograde axonal transport and what things is it important for

A

cell body nutrients are carried to the distal end
vital for axonal growth during development, maintenance of axonal structure, synthesis and release of NTs

37
Q

what is retrograde axonal transport and what is it important for

A

distal end of axon back to cell body
return of used materials from the terminal to the cell body for restoration and reuse
route by which toxins enter the CNS from periphery

38
Q

what does axonal transport do

A

maintains the integrity of the axon

39
Q

explain the effects of tetanus and how it enters the CNS
what muscles does tetanus first attack and what symptoms does this lead to
is tetanus localized or general

A

causes increase in tone and spasms, inhibits motor neurons of the CNS
enters the CNS through retrograde axonal transport
attacks facial and jaw muscles
stiffness of the neck, difficulty swallowing, stiffness in abdominal musculature
can be either localized or general

40
Q

what can interfere with transmission and are these effects direct or indirect

A

drugs, toxins, endogenous compounds, injuries or diseases
can be either direct or indirect

41
Q

what is myasthenia gravis
what receptors does it affect and what does this condition lead to
what is the treatment for this

A

an acquired autoimmune disorder affecting transmission at the NMJ
affects nicotinic ACh receptors
leads to skeletal muscle weakness and fatiguability in orbital, oropharyngeal and limb musculature
acetylcholinesterase inhibitors (would allow for an increase in the amount of ACh)

42
Q

what NT is active at the NMJ
what is botulinum toxin and how does it affect this NT at the NMJ
botulinum toxin can be used as a treatment for what conditions

A

ACh
a bacteria that prevents the release of ACh at the NMJ and causes flaccid paralysis which can be fatal
severe dystonia or cerebral palsy (both have muscle contractures so the bacteria relaxes these contractures)

43
Q

describe each type of nerve injury and their characteristics (damage, paralysis vs block, wallerian degeneration, example, recovery)

A

neurapraxia: damage to the sheath but neuron still intact, block in conduction, no wallerian degeneration, compression injury, fast recovery
axonotmesis: axon and sheath damaged but connective tissue intact, paralysis, wallerian degeneration, stretch injury, slow recovery
neurotmesis: complete nerve damage, paralysis, wallerian degeneration, trauma, recovery may not be possible (may require surgery)

44
Q

damage to which part of the neuron would make recovery impossible
loss of ___ is irreparable but ___ can regenerate if cell body is intact

A

cell bodies
neurons, axons

45
Q

regeneration of axons is limited to axons in the CNS or PNS
what can assist in repairing an axon to regrow
what can occur if there is an issue during the repair of a neuron

A

PNS
Schwann cells
develop a neuroma (thickening of nerve tissue and enlargement)

46
Q

what conditions may cause muscle atrophy
what does denervation of muscles lead to
is muscle atrophy reversible

A

injury, acute critical illness, cancer, diseases with chronic inflammation, neurological disorders, long term corticosteroid therapy
muscle fibre death and muscle atrophy, changes in metabolism or morphology and transmitter receptor production
may be reversible depending on the cause and duration of illness

47
Q

intensive care unit acquired weakness (ICUAW) is caused by what
what happens to the vascular permeability of the endometrium in ICUAW and what does this allow

A

axonal neuropathy, myopathy or both
increases in permeability allowing toxins to penetrate in the nerve ends

48
Q

what does mechanical ventilation in the ICU change the balance between
what can help reduce the severity of ICUAW

A

protein synthesis and protein degradation (changes fibre composition of the diaphragm)
mobility, passive stretching, electrical stimulation

49
Q

what is neuropathy and what are the causes of it
give an example of a focal neuropathy

A

damage to peripheral nerves that result in sensations of numbness, weakness, tingling or pain
most common cause is diabetes but can also be infectious/inflammatory diseases, exposure to toxic substances
carpal tunnel syndrome

50
Q

what is Guillain barre syndrome
what is Charcot Marie tooth disease
what is MS

A

an acquired, acute onset inflammatory peripheral demyelinating neuropathy with axonal sparing
hereditary polyneuropathy with demyelination of sensory and motor axons
an acquired demyelinating disease of the CNS

51
Q

what changes do we see presynaptically with synaptic plasticity
what changes do we see postsynaptically with synaptic plasticity

A

pre: increase in size of presynaptic terminal, number of axon terminals, quantity of NTs in vesicles
post: increase in the receptor zone, in the number of receptors, growth of dendritic spines

52
Q

how can chronic stress affect synaptic plasticity differently in different areas of the brain

A

pruning in the prefrontal cortex which can impact memory and learning
amygdala (emotions and fear response) develops more connections and we have exaggerated responses to fearful situations

53
Q

describe what makes a stress positive, tolerable or toxic

A

positive: necessary for development and to enable stable and supportive relationships (exercise)
tolerable: potentially disruptive, buffered by supportive relationship and safe environments (school)
toxic: disrupts brain architecture, increases risk of stress related physical and mental illness (burnout)

PT 9111 (23 decks)

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