5 The Neuromuscular Junction and Muscle Contraction Flashcards
Q: What is the neuromuscular junction? allows? Responsible for?
A: specialised synapse between a motor neuron and a muscle fibre
allows unidirectional communication before peripheral nerve and muscle
initiating muscle contraction
Q: What’s the structure of a standard chemical synapse? Role of specific vesicles?
A: presynaptic axon
presynaptic terminal (bouton) containing synaptic vesicles (propogate change in membrane potential -> carry AP)
synaptic cleft
postsynaptic membrane containing receptors
Q: What’s the structure of a neuromuscular junction? 3 main structures? Specific to striated muscle?
A: REFER
axon with myelin sheath and schwann cell right at end just before widening of terminal
flat presynaptic terminal contains mitochondria, achetylcholine containing vesicles
-> has voltage gated calcium channels
small synaptic cleft with highly folded post synaptic muscle membrane
membrane has ACh receptors at tops of folds and achetylcholinesterase in clefts
- presynaptic nerve terminal
- synaptic cleft
- postsynaptic endplate region on the muscle fibre
ACh serves as the NT for voluntary striated muscle
Q: Label a spinal cord cross section. (7)
A: REFER
dorsal/posterior
CS
anterior/ventral
- grey matter = within in butterfly shape (wider wings at ventral end)
- white matter around it
- posterior/dorsal root coming out of back= sensory fibres entering AND CONTAINS BULGE= ROOT GANGLIAN which contains body of sensory neuron
- anterior/ventral root coming out front = motor fibres (cell bodies reside in anterior horn of grey matter)
=> connect to make mixed nerve
Q: How do muscle fibres vary in terms of innnervation?
A: muscle fibres that are innervated by certain branches of the motor neuron are not fibres innervated by sensory neurons
under normal conditions, a neuron, can go to multiple muscle fibres but those muscle fibres will not be innervated by any other neurone
Q: What are the 7 steps in NMJ function? Result?
A: 1. Action potential reaches presynaptic terminal= opens V-gated Ca2+ channels
- Ca2+ enters
- Ca2+ triggers exocytosis of vesicles SNARE
- 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
activate structures within skeletal muscle and cause contraction
Q: What’s the SNARE protein?
A: complex responsible for making membrane of vesicle fuse with membrane of nerve terminal-> contents of vesicle are emptied into synaptic cleft
Q: What occurs to NMJs at rest? causes? not? Variation?
A: release vesicles of ACh at v slow rate causing miniature end-plate potentials (MEPs)
don’t result in depolarisation of membrane = no contraction
vesicles contain specific (discrete) amounts of ACh
Q: What structure of muscle cell membranes aids conduction?
A: invaginations of membrane= produce T tubules that convey AP deep into muscle so that all muscle fibres can contract in muscle
Q: Describe cells of skeletal muscle? contain which essential organelle?
A: cells have merged to create multinucleated fibres
myofibrils
Q: What’s the structure of myofibres? (5) composed of?
A: -Covered by plasma membrane – sarcolemma
- T-tubules tunnel into centre
- Cytoplasm called sarcoplasm
- myoglobin and mitochondria present
- Network of fluid filled tubules – sarcoplasmic reticulum: Ca store -> released to allow contraction
Composed of myofibrils
Q: What are myofibrils? composed of? Diameter? Where are they?
A: any of the elongated contractile threads found in striated muscle cells
of two main types of protein – actin and myosin
1-2μm (10^-6) in diameter
Extend along entire length of myofibres
Q: What are microfilaments? Appearance? Where are they? Arrangement?
A: filaments of myofibrils
Light and dark bands give muscle striated appearance
Do not extend along length of myofibers
Overlap and are arranged in compartments called sarcomeres
Q: What is the structure of sarcomeres? (3)
A: dense protein Z discs separate sarcomeres
dark bands- A band (thick-myosin and mix)- stays same size
light bands- I band (thin-actin only)
Q: What are the sarcomere observations with the sliding filament theory? (3)
A: During contraction I band became shorter
A-band remained same length
H-zone narrowed or disappeared
Q: Explain the activation and relaxation process of the sliding filament theory. (8)
A: 1. Action potential propagates along surface membrane and into T-tubules
- DHP (dihydropyridine) receptor in T-tubule membrane: senses change in V = causing a conformational change in DHPR -> allows DHPR to make physical contact with…
- conformational change means that Ryanodine receptor opens = 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
Q: Describe disorders of NMJ. causing? Examples? (3)
A: Pathological processes interfering with NMJ function can cause muscle weakness
- Botulism
- Myastenia gravis (MG)
- Lambert-Eaton myastenic syndrome (LEMS)
Q: What is botulism? What’s prevented? What do you get?
A: Botulinum toxin from bacteria produces an irreversible disruption in stimulation-induced acetylcholine release by the presynaptic nerve terminal- prevents Ca2+ influx
just get relaxation
Q: What causes Myastenia gravis (MG)? History? What does it cause? (2) Diagnosis? (2) Severe case treatment? allows?
A: An autoimmune disorder where antibodies are directed against the acetylcholine receptor
There may be a personal or family history of other autoimmune diseases
fatigable weakness (i.e. becomes more pronounced with repetitive use) and may affect the ocular, respiratory or limb muscles
Antibodies are detected in nearly 90% of cases and EMG examination will confirm the diagnosis
antibodies in the blood can be removed via plasma exchange (plasma without antibodies) which allows rapid improvement to occur.
Q: What is Lambert-Eaton myastenic syndrome (LEMS)? associated with? Causes?
A: an autoimmune disease caused by antibodies directed against the voltage-gated calcium channel (VGCC) - associated with lung cancer
failure of neurotransmission, no AP created
