NMJ, muscle contraction Flashcards
NMJ is between?
between a motor neuron and a muscle fibre
NMJ label
(slide 4, lecture 5)
Main structures
Main structures
presynaptic nerve terminal
synaptic cleft
postsynaptic endplate region on the muscle fibre
Allows for?
unidirectional chemical communication between peripheral nerve and muscle
Acetylcholine role?
NT for voluntary striated muscle
single muscle fibre will have innervation from
a branch of a SINGLE MOTOR neurone only
(not both afferent/ efferent)
In injury this isn’t the case so can differentiate between injured muscle
Types of motor neurones
Upper (brain)
Lower (brainstem+ spinal cored)
Afferent neurones bring information into cord through
Dorsal route (dorsal ganglion)
Efferent neurones take information out of cord in
anterior horn (grey body of spinal cord)
Process when action potential reaches NMJ
- Action potential open V-gated Ca2+ channels
- Ca2+ enters
- Ca2+ triggers exocytosis of vesicles
- Acetylcholine diffuses in cleft
- Acetylcholine binds to receptor-cation channel & opens channel
- Local currents flow from depolarized region and adjacent region; action potential triggered and spreads along surface membrane
- Acetylcholine broken down by acetylcholine esterase (enzyme). Muscle fibre response to that molecule of Acetylcholine ceases
Normal physiology of NMJ
Individual vesicles release ACh at a very low rate causing miniature end-plate potentials (MEPPs)
Skeletal muscle structure
slide 10, lecture 5
-
Myofibres- composition
Covered by?
Cytoplasm=?
Composed of?
Covered by plasma membrane – sarcolemma
T-tubules tunnel into centre
Cytoplasm called sarcoplasm – myoglobin and mitochondria present
Network of fluid filled tubules – sarcoplasmic reticulum
Composed of myofibrils
Myofibrils
Diameter
Composed of?
1-2μm in diameter
Extend along entire length of myofibres
Composed of two main types of protein – actin and myosin
Myofilaments
Light and dark bands give muscle striated appearance
Do not extend along length of myofibers
Overlap and are arranged in compartments called sarcomeres
Cnocentric contraction
muscle gets shorter
Eccentric contraction
muscle gets longer
Myofilaments
Dense protein Z-discs separate sarcomeres
Dark bands – A band (thick - myosin)
Light bands – I band (thin - actin)
Myosin and actin filaments overlap
Sliding filament theory changes in bands
I band became shorter
A-band remained same length
H-zone narrowed or disappeared
Muscle activation process
- Action potential propagates along surface membrane and into T-tubules
- DHP (dihydropyridine) receptor in T-tubule membrane: senses ΔV & changes shape of the protein link to Ryanodine receptor, opens the Ryanodine receptor Ca2+ channel in the SR membrane; Ca2+ released from SR into space around the filaments
- Ca2+ binds to Troponin & Tropomyosin moves allowing
- Crossbridges to attach to actin
- Ca2+ is actively transported into the SR continuously while action potentials continue. ATP- driven pump (uptake rate < or = release rate).
- Ca2+ dissociates from TN when free Ca2+ declines; TM block prevents new crossbridge attachment; Active force declines due to net crossbridge detachment
Disorders of NMJ
Botulism
Botulinum toxin produces an irreversible disruption in stimulation-induced acetylcholine release by the presynaptic nerve terminal
Stops the release of acetylcholine into the synaptic cleft
Myastenia gravis (MG) An autoimmune disorder where antibodies are directed against the acetylcholine receptor (Acetylcholine gets to the receptor but the receptor doesn’t bind to it (binds to antibody instead)
Lambert-Eaton myastenic syndrome (LEMS)
an autoimmune disease caused by antibodies directed against the voltage-gated calcium channel (VGCC) - associated with lung cancer.
Muscle doesn’t contract because action potential arrives to muscle but Ca Induced Ca Release
