Human respiration is dependent upon the interaction of acetylcholine molecules with acetylcholine esterase receptors on the diaphragm muscle. Each time a person takes a breath, nerve endings that contain "sacks" of acetylcholine are stimulated. Each sack has roughly 1 x 1014 acetylcholine molecules inside. The sacks move toward the end of the nerve and eventually strike the wall of the nerve. The force of the collision causes the sacks to release the acetylcholine molecules into the neuromuscular junction or synapse.
The acetylcholine molecule has a positive nitrogen group which is attracted to the negative charge of an acetylcholine esterase receptor site on the diaphragm.
The attraction between the molecule and a receptor site causes a bridging to occur, and a channel for impulses from the nerve to the muscle is opened. Each interaction with the receptor site causes the channel to open for approximately 400 microseconds . The opening of the channel allows for the transmission of an electrical impulse that stimulates the contraction of the muscle fiber. Many of these neuromuscular interactions combine to create a uniform muscle response; i.e., a contraction of the diaphragm, which is the driving force behind human respiration. Each breath a human takes is a result of the interaction described above.
The acetylcholine molecule contains an ester group which reacts with the alcohol group of the receptor site. This reaction is responsible for the degradation of the acetylcholine molecule.
Once the molecule is broken down, a reaction with water occurs and the receptor site releases the molecules. Once the molecules are released, the impulse channel closes and the receptor site is free to interact with another acetylcholine molecule.
The molecules that are released from the receptor site are then used by the body to form new acetylcholine molecules that are again stored in the sacks in the nerve ending.
Since the body produces the acetylcholine molecule, the process is cyclic
in nature and self-sustaining. The process will continue to occur until
something prohibits the interaction with the receptor site and stops the
formation of the acetylcholine molecule.
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