From nerve impulse to calcium.

Follow the signal upstream of the sarcomere: motor neuron fires, acetylcholine crosses the end plate, the sarcolemma action potential makes the sarcoplasmic reticulum release Ca2+; block the ACh receptors (myasthenia gravis) or drop body-fluid Ca2+ (tetany) and see what fails.

Produce a smooth sustained contraction, then reproduce the weakness of myasthenia gravis and the spasms of tetany with one control each.

Ca2+ binds tropomyosin or myosin; tetany confused with myasthenia gravis.

• The sliding filament theory explains contraction: a muscle fibre shortens because the thin filaments slide over the thick filaments.
• The CNS starts contraction by sending a signal along a motor neuron. A motor neuron with the muscle fibres it supplies is a motor unit.
• The junction between a motor neuron and the sarcolemma is the neuromuscular junction, or motor end plate. There the signal releases the neurotransmitter acetylcholine, which sets up an action potential in the sarcolemma.
• The action potential spreads through the fibre and causes calcium ions to be released into the sarcoplasm.
• Ca²⁺ binds a subunit of troponin, which uncovers the active sites for myosin on actin.
• Using energy from ATP hydrolysis, the myosin head binds the exposed sites to form a cross bridge, and pulls the attached actin filaments towards the centre of the A band.
• The Z lines attached to those actins are pulled inwards too, so the sarcomere shortens. During contraction the I bands shorten while the A bands keep their length.
• The myosin head releases ADP and Pi and returns to its relaxed state; a fresh ATP binds and the cross bridge breaks. The ATP is hydrolysed again and the cycle of making and breaking cross bridges repeats, sliding the filaments further.
• This goes on until Ca²⁺ is pumped back into the sarcoplasmic cisternae, the actin sites are covered again, and the Z lines return to their original place: relaxation.

Teaching this idea? Put the simulation on your own page or LMS with this code.