Action potential travels down the axon in response to nerve stimulus.
Action potential travels down the T Tubule and into Sarcoplasmic Reticulum (SR)
Action potential causes Ca2+ release from SR
Ca2+ binds to troponin. Troponin moves tropomyosin uncovering myosin binding site on actin
Myosin binds to actin
Myosin pulls actin chain along and Sarcomere shortens leading to contraction!
Ca2+ pumps restore Ca2+ to SR relaxation!
At synaptic junctions:
The action potential travels along the membrane until the synapse where it’s electrical depolarization leads to the opening of channels allowing only sodium ions to enter
these flow through a presynaptic membrane until the concentration is built up, activating ion sensitive proteins attached to vesicles containing neurotransmitters like acetylcholine
this leads to changes in the proteins leading to the fusion with the membrane of the presynaptic cell, so vesicles are open and neurotransmitter is released. The neurotransmitter diffuses across to chemical receptors on the presynaptic cell where they bind temporarily. This increases the permeability of the sarcolema to Na+;a new action potential is generated
This action potential in the muscle, travels along T-tubules, and Ca+ ions are released by the sarcoplasmic reticulum into the sarcoplasm
Ca and troponin combine, pulling myosin filaments, exposing the actin filament's myosin binding sites
cross-bridge formation occurs, leading to the sliding of filaments. ACH degraded in the synapse. Na ions are not released, and the action potential is not transmitted.
the Ca channels on the SR close, while Ca is reabsorbed stopping Ca-troponin binding, closing myosin binding sites on actin and leading to cross bridge separation. The muscle fiber relaxes in their resting states.
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