Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IMS Nerves and muscles > 3 NMJ > Flashcards

3 NMJ Flashcards

1
Q

motor unit consists of

A

the motor nerve and all the muscle fibres innervated by that nerve

all the muscle fibres within a motor unit contract together when the motor nerve fires

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

size of motor unit varies

A

depends on function of the muscle innervated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

individual innervation of fibre

A

each individual muscle fibre is separately innervated by the nerve (no gap junctions between fibres) so has t have direct contact via NMR

more fibres innervated = stronger contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

1:1 transmission means

A

chemical transmission which is designed so that every presynaptic action potential results in a postsynaptic one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

time delay of transmission across NMJ

A

0.5-1ms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

NMJ easily affected by

A

drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

NMJ location

A

synapse between motor neuron and skeletal muscle fibres = bridges gap as they do not touch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how CNS links to NMJ

A

Motor nerve cell bodies sited in the ventral horn of the spinal cord send out axons via ventral roots to innervate the appropriate muscles

These axons are myelinated as they pass through the CNS and into the peripheral nerves but divide to supply thin unmyelinated fibres, which can each innervate several individual muscle fibre cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

nAChR’s =

A

nicotinic acetylcholine receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

nicotinic vs muscarinic

A

nicotinic = ionotropic receptor

muscarinic = metabotropic receptor (GPCR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cholinergic (receptor)

A

responds to ACh binding

2 types:

  • nicotinic = nAChR
  • muscarinic = mAChR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

basal lamina

A

support within the synaptic cleft = AChE is attached to

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

structure of nAChR’s

A
  • formed from 5 subunits

- each subunit formed from 4 transmembrane segments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

nAChR’s have different subunit types

A

so different types of nAChR depending on composition = affects pharmacological profile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

subunits in nAChR’s

A

5 subunits total = heteromeric receptor

2 alpha
1 beta
1 gamma
1 delta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

(2) alpha subunits in nAChR’s

A

= have ACh binding sites – 2 molecules of ACh must bind to receptor before receptor is activated (one on each alpha subunit)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

MEPPs

A

Miniature End Plate Potentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

1 quantum

A

= contents of 1 synaptic vesicle (5000 molecules of ACh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is an MEPP

A

ACh released as a random event (i.e. no action potential or calcium influx necessary) – smallest measurable event in transmission = don’t get parts of quanta released, either 1 quantum or multiples of 1

20
Q

many MEPPs together

A

= when action potential causes release of many vesicles, forms EPP – generates action potential

21
Q

inactivation of ACh

A

ACh hydrolysed by AchE

22
Q

products of hydrolysis of ACh

A

ACh -> acetate + choline

choline is reabsorbed by presynaptic cell

acetyl CoA + choline -> acetylcholine + CoA

(acetate + CoA -> acetyl CoA)

23
Q

docking of vesicles containing ACh

A

v-snare protein on Vesicle binds with t-snare on presynaptic membrane

24
Q

get ACh into vesicle

A

co-transport H+ out, ACh in

25
Q

agonist

A

binds to the receptor and produces an effect within the cell

26
Q

antagonist

A

binds to receptor and blocks response

27
Q

nAChR antagonist = non-depolarising

A

tubocurarine

28
Q

drugs used at NMJ:

blocking agents can be depolarising or non-depolarising

A

depolarising

non-depolarising = no APs generated

29
Q

action of tubocurarine

A

competes with Ach for nicotinic receptor binding sites

30
Q

effect of tubocurarine at NMJ

A

muscle paralysis occurs gradually

therapeutic use = surgery as an anaesthetic

onset =5 mins
duration 30 mins

31
Q

adverse effects of tubocurarine

A

hypotension (increases histamine release, a vasodilator)

bronchospasm

32
Q

reversal of tubocurarine

A

increase ACh conc in synaptic cleft

= AChE inhibitors

33
Q

nAChR agonist = persistent depolarising

A

succinylcholine

34
Q

action of succinylcholine

A

persistent depolarization of the neuromuscular junction = motor end plate

works similar to ACh but is longer acting (as is broken down less rapidly)

35
Q

effect of succinylcholine

A

phase I:
= membrane depolarized causing brief period of muscle fasciculation (twitching)

phase II:
(desensitizing phase)
= end-plate eventually repolarizes, but because succinycholine is not metabolized like ACh it continues to occupy the AChRs to “desensitize” the end-plate

The muscle is no longer responsive to ACh released by the motoneurons. At this point, full neuromuscular block has been achieved.

=Flaccid paralysis

36
Q

adverse effects of succinylcholine

A

when administrated with halothane genetically susceptible people experience malignant hyperthermia

37
Q

reversal of succinylcholine

A

hydrolysed by esterases

38
Q

therapeutic use of succinylcholine

A

surgery continuous IV

short acting

39
Q

cholinesterase inhibitor examples (2)

A

Neostigmine, edrophonium

40
Q

mechanism of cholinesterases

A

inhibits AChE

41
Q

therapeutic uses of cholinesterase inhibitors

A

Antidote for non depolarising blockers such as Tubocurarine
Treatment for myasthenia gravis (neostigmine)
Diagnosis of myasthenia gravis (edrophonium)

42
Q

adverse effects of AChE inhibitors

A

Abdominal cramping, diarrhoea, salivation, incontinence, actions on paraSymp NS, hypotension, bradycardia, GI tract hypermotility, bronchoconstriction

43
Q

sarin weapon action

“nerve gas”

A

AChE inhibitor

  • muscles can contract in powerful convulsive reactions
  • nose and eyes can water severely and drooling
  • nausea and vomiting
  • constriction of the pupils to pinpoints
  • loss of control of bowel and bladder can follow
  • chest pain, shortness of breath, collapse, seizures
  • > death is the end result
44
Q

toxin effects at NMJ = Tetanus and botulinum

A

prevent vesicles binding to presynaptic membrane

45
Q

action of botulinum toxin

disease = botulism, caused by bacteria

A

cleaves SNARE proteins = involved with fusing synaptic vesicles to the plasma membrane
= inhibits the release of acetylcholine at NMJ

-> flaccid paralysis

IMS Nerves and muscles (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions