When curare, a neuromuscular poison, is dropped onto an isolated muscle-nerve preparation in a laboratory, the muscle does not contract when the nerve is stimulated, even though neurotransmitter is released from the nerve cell. Why does this happen? How might this action of curare be lethal to an individual who has been poisoned?

When an action potential arrives at the neuromuscular junction, acetylcholine is released into the synaptic cleft and binds to receptors in the postsynaptic membrane. Which of the following represents the correct order of the next series of events?   A. An action potential travels down the T tubules, depolarization spreads through the T tubules, Ca2+ is released from the sarcoplasmic reticulum, and myosin binds to actin.   B. Ca2+ is released from the sarcoplasmic reticulum, an action potential travels down the T tubules, depolarization spreads through the T tubules, and myosin binds to actin.   C. An action potential travels down the T tubules, depolarization spreads through the T tubules, Ca2+ is taken up by the sarcoplasmic reticulum, and myosin binds to actin.   D. T tubules are depolarized, Ca2+ is released from the sarcoplasmic reticulum, an action potential is created in the muscle cell, and myosin bonds to actin.   E. An action potential travels…

Sarin is an inhibitor of acetylcholinesterase. Draw a mechanism that shows this.

Lower back pain is quite common in America and treatments for this pain include muscle relaxants. How does the drug cyclobenzaprine work as a muscle relaxant at a cellular level? Which part of the muscle contraction is interrupted by cyclobenzaprine? Is it effective on the muscle itself or active in the central nervous system?