Excitation of Skeletal Muscle: Neuromuscular Transmission & Excitation-Contraction Coupling Flashcards
•Highly branched nerve fiber outside of muscle fiber plasma membrane
Motor End Plate
Synthesized in cytoplasm of neuron using ATP
Found in synaptic vesicles
Acetylcholine
vesicles/end plate
300,000
located in synaptic cleft
in synaptic space degrades ACH to acetyl-CoA & choline
Acetylcholinesterase
Nerve impulse reaches neuromuscular junction
Ca2+ channels open & flux into presynaptic terminal
Ca2+ attract ACH vesicles to membrane next to dense bars
125 vesicles fuse with terminal membrane
Acetylcholine (ACH) Secretion
•Chemical-gated ion channels
•Small diameter & negatively charged amino acids (acidic) at mouth = keep out negative ions
•Na+, K+ & Ca2+ have the ability to diffuse through
•In reality, Na+ almost exclusively flows through
•Stimulates contraction of muscle
Hall.
ACH receptors
Na+ influx creates positive potential charge =
end plate potential
ACH receptors
Localized
Can be weakened & not reach threshold levels with some meds & toxins (botox)
•End result = paralysis
neuromuscular junction is 3x as much end plate potential
fatigue Due to utilization of most ACH vesicles
End Plate Potential
Nerve gases & Alzheimer’s meds
•Decreased breakdown of ACH
Binds ACH receptors, so ACH can’t
Acetylcholinesterase inhibitors
Drugs that Affect the Neuromuscular Junction
Increase GI secretions & urination, pupil constriction Anticholinergic: reduce GI secretions & motility, inc. heart rate, dec. lung secretions, urine retentions, pupil dilation
muscarinic receptor
Increased heart rate, blood pressure & GI activity
Blockers: hypotension, dec. GI secretions & motility, dec. urination
nicotinic receptor on autonomic ganglia
Depolarization & muscle contraction
Blockers: muscle relaxation
nicotinic receptor on autonomic ganglia
Nausea, vomiting, diarrhea, blurred vision, tremors, hypotension, bronchoconstriction
Cholinergic
Dry mouth, urinary retention, constipation, flushing, fever, depression, tachycardia
Anticholinergic
Nausea, vomiting, diarrhea, headache, confusion
Anticholinesterases
Altered taste, nausea, heartburn
Nn agonist
Dry mouth, constipation, hypotension, impotency
Nn blocker
Paralysis of respiratory muscles
Nm blocker
Antibodies attack ACH receptors at neuromuscular junction
Inability to transmit enough signals from nerves to muscles
Myasthenia Gravis
Does not penetrate into fiber
Action potential transmitted along transverse tubules (T tubules
T tubules penetrate into muscle fiber
Stimulate release of Ca2+ & contraction
Muscle Action Potential
One end open to extracellular fluid
•Electrical current that spreads over muscle fiber
Transverse (T) Tubule
Excitation-Contraction Coupling
action potential reaches T tubule next to sarcoplasmic reticulum
Calcium release stimulates contraction
Ca2+ release from sarcoplasmic reticulum
in sarcoplasmic reticulum pump Ca2+ back in
Calcium pump
Ca2+ concentration increases 500x
(10x more than level for maximum contraction)
This pulse of Ca2+ lasts ~1/20 second
Calcium ‘Pulse’
