Physiology of NMJ Flashcards
are the axons of motor neurones innervating skeletal muscles myelinated or unmyelinated
both starts myelinated then branches into unmyelinted branches near the muscle
what is a terminal bouton
end of nerve branch that forms a synapse with the muscle membrane at the NMJ
what causes the release of acetylcholine
the conduction of action potentials that arise in the cell via the axon to the boutons
who transmits faster myelinated or unmyelinated
myelinated
what is the neurotransmitter of all motor neurones of skeletal muscle
acetylcholine (ACh)
what type of motor neurone innervates skeletal muscles
alpha
what part of spinal chord does does myelinated alpha neurone arise from
ventral body of spinal chord
where does the pre synaptic terminal bouton synapse
the endplate region of the skeletal muscle fibre
what surrounds terminal boutons
schwann cell
what are the components of the NMJ
terminal bouton
surrounding schwann cells
synaptic vessels
synaptic cleft
end plate region of the muscle cell membrane (sarcolemma)
what is the sarcolemma
the end plate region of the muscle cell membrane
what is the synaptic cleft
the space between neurones at a nerve synapse across which a nerve impulse is transmitted by a neurotransmitter (aka synaptic gap)
what do synaptic vesicles contain
ACh
where do synaptic vesicles cluster
active zones
where are nicotinic ACh receptors located
at regions of the junctional folds that face the active zones
what are the components of ACH
choline and acetylCoA (from acetate)
when does the release of ACh from vesicles occur
when the action potential opens voltage activated Ca++ channel
how is choline transported into the terminal
choline transporter (symport with Na+)
describe the synthesis of ACh
happens in cytosol
from choline and acetyl coenzyme A (supplied by mitochondia) by the enzyme choline acetyltransferase (CAT)
what concentrates ACh in the vesicles
vesicular ACh transporter
what does arrival of the action potential at the terminal cause
depolarisation and the opening of voltage activated Ca++ channels - this allows calcium entry to the terminal
what happens to the vesicles when calcium is released
fuse with the presynaptic membrane (exocytosis) causing ACh to diffuse into the synaptic cleft
what does the diffusion of ACh in the synaptic cleft do
activates post synaptic nicotinic ACh receptors in the muscle endplate region
what are nicotinic ACh receptors made of
a pentamer of glycoprotein subunits which surround a cation sensitive pore (opens in the presence of ACh)
what happens when nicotinic ACh receptors open
Na+ enter the muscle cell whilst K+ exits = depolarisation called the end plate potential (e.p.p)
what is the miniature endplate potential
the electrical response to one ‘quantum’ of transmitter released from a vesicle - summate to produce the e.p.p
what does e.p.p do when it exceeds a threshold
triggers the opening of voltage activated Na+ channels which causes a propagated action potential that initiates contraction
what type of response is the e.p.p
graded response
where does action potential propagate in the skeletal muscle cell
sarcolemma (surface membrane) then enters transverse T tubules
what does action potential arriving at T tubule trigger
release of calcium from SR- which in turn causes contraction by interacting with troponin associated with the myofibrils
what terminates the action of ACh
acetylcholinesterase- hydrolyses ACh into choline (taken up by choline transporter) and acetate (diffuses from the synaptic cleft)
Neuromytonia :
what are the symptoms
what causes it
treatments
cramps, stiffness, slow relaxation, muscle twitches
antibodies against voltage activated K+ channels
anticonvulsants
lambert eaton myasthenic syndrome:
symptoms
cause
treatment
muscle weakness
antibodies against voltage activate Ca++ channels
anticholinesterases, potassium channel blockers
myasthenia gravis:
symptoms
causes
treatment
progressive muscle weakness during periods of activity
antibodies against nicotinic ACh receptors
anticholinesterases, immunosuppressants
what do anticholinesterases do
increase conc of ACh in synaptic cleft
what does botox (botulinum toxin) do
acts at motor neurone terminals to irreversibly inhibit ACh release
what do curare like compounds do
competitive antagonists of ACh receptors, reduce amplitude of e.p.p
used clinically to induce reversible muscle paralysis
