Excitation of Skeletal Muscle Flashcards
Secretion of Acetylcholine by the Nerve Terminals
- Nerve impulse reaches nueromuscular junction
- AP spreads over terminal, voltage gated Ca channels open and allow Ca++ to diffuse from synaptic space to the interior of the nerve terminal.
- Ca ions exert an attractive influence on the ACh vesicles drawing them to the neural membrane where they empty their ACh into the synaptic space by exocytosis
ACh Receptor
- A postsynaptic membrane of the motor end plate
- Remaints constricted until two ACh molecuels attach to two alpha subunit proteins
- Causes channel to open and allows Na K and Ca to move easily through the opening
- Cl- do not pass through through because of strong negative charges in the mouth of the channel that repel these negative ions
- More Na+ flow through than any other ions
- large concentration
- very negative potential on the inside of the muscle membrane (-80 - -90 mV) pulls the positively charged Na+ ions to the inside of the fiber while preventing efflux of the + K+ ions
- Creates a local positive potential change inside hte muscle fiber membrane called the end plate potential - initiating an AP that spreads along the muscle membrane -> contraction
Destruction of Released ACh
- Most of ACh is destroyed by the enzyme acetylcholinesterase
- A small amount of ACh diffuses out of the synpatic space
Rapid removal of the ACh prevents continued muscle re-excitation after the muscle fiber has recovered from its initial AP
End Plate Potential
Self regenerative effect of more and more sodium ions flowing to the interior of the fiber initiates an action potential
Effects of drugs
Curare - blocks the gating action of acetylcholine on the ACh channels by competiing for ACh receptor spots.
Botox - Decreases the quanity of acetylcholine release by the nerve terminals
- Both result in weak end plate potentials (weak local end plate voltage changes) that do not initiate an AP
Safety Factor for Transmission
Each impulse that arrives at the neuromucular junction causes about three times as much end plate potential as that required to stimulate the muscle fiber
Stimulation at rates greater than 100 times per second for serveral minutes often diminishes the number of ACh vesciles so much that impulses fail to pass into the muscle fiber = Fatigue
Myasthenia gravis
Causes muscle paralysis because of inability of the neuromuscular junctions to transmit enoguh signals from the nerve fibers to the muscle fibers
- Antibodies attack the ACh gated sodium ion transport proteins
- autoimmune disease
- end plate potentials too weak to stimualte muscle fibers
Transverse Tubules
Spreads the AP to the interior of the muscle fiber
- penetrate all the way through the muscle fiber from one side of the fiber to the other
- The T tubule APs cause release of calcium ions inside the muscle fiber –> contraction
- excitation-contraction coupling
T tubule - SR system
Myofibrils are surrouned by the T tubule-sacroplasmic reticulum system
- Where the tubules originate from the cell membrane, they are open to the exterior of the muscle fiber therefore they communicate with the extracellular fluid
- AP spreads over a muscle fiber membrane, a potential change also spreads along the T tubules to the deep interior of the muscle fiber
SR
- Large chamers called termnial cisternae that abut the T tubules
- long longitiudinal tubules that surround all surfaces of the actual contracting myofibrils
Release of Ca by SR
Excess of Ca++ ions in its vesicular tubules that are released when an AP occurs in the adjacent T tubule
- AP of the T tubule causes current flow into the sacroplasmic reticular cisternae where they abut the T tubule
- This causes rapid opening of large numbers of calcium channels through the membranes of the cisternae as well as their attached longitiudinal tubules
Calcium pump
removes Ca++ ions from the myofibrillar fluid after contraction occurs
- a continually active Ca pump located in the walls of the sacroplasmic reticulum pumps Ca++ ions away from the myofibrils back into the SR tubules