Your muscles are composed of many motor units, which comprise muscle fibers. Muscles contract after an electrical impulse from your brain or other source stimulates the muscle at a place called the neuronal synapse; this is where the electrical signal is turned into a chemical signal. The electrical impulse arrives at the terminal of the neuron, called the neuromuscular junction (NMJ), activating the chemical signal by releasing neurotransmitters from the neuron.
The neurotransmitters cross the space between the neuron and the muscle fiber and bind to receptors. The neurotransmitters are then cleared to avoid over-stimulation and to allow the synapse to be activated again. For example, when you step on a sharp nail, an electrical impulse is sent from your sensory neurons (which sense pain) to your spinal cord, where the impulse is transfered to a motor neuron (which signal muscles to take action). The signal arrives at the place where neuron meets muscle, the NMJ. This is where the electrical signal is translated to a chemical signal, a "language" that muscles can "understand" and respond to.
To start the process, a nerve impulse from a neuron originating in the brain or a sensory neuron in your foot, for example, is stimulated by your brain or your foot after you step on a nail. The nerve impulse must reach the neuromuscular junction, which is the synapse between the motor neuron and the skeletal muscle fiber of your quadriceps in our painful nail example.
The neurotransmitter used at NMJs is acetylcholine (ACh). This is the chemical messenger that must cross from the neuron into the synaptic cleft. ACh is packaged in vesicles that must fuse with the neuron's membrane. This allows the ACh to be released into the synaptic cleft. ACh then diffuses across the cleft towards the motor end plate (the muscle fiber portion of the NMJ).
Acetylcholine Receptors Activated
ACh then binds to receptors on the motor end plate. This opens an ion channel in the ACh receptor. Small cations (positively charged ions, such as Na+) flow across the membrane through these newly opened channels. The electrical signal from your neuron is now being converted to a chemical signal, the stimulus of muscle contraction.
Action Potential Produced
The muscle fiber is now receiving Na+, which makes the inside of the muscle fiber more positively charged. This triggers a muscle action potential, which leads to a contraction of the muscle fiber; a more positively charged or depolarized muscle fiber forms the basis of how muscles contract.
Acetylcholine Activity Terminated
The binding of receptors is short lived, however, because the acetylcholine that is binding the receptors is quickly broken down. After you have lifted your leg to lift your foot off the nail, the ACh must be removed from its receptor so your leg muscles can relax. The enzyme that accomplishes this task is called acetylcholinesterase. Acetylcholine is broken down by this enzyme to acetyl and choline, two products that cannot activate the receptor alone. This ensures that the receptor is not perpetually activated, which would make muscles contract indefinitely (this is the physiological basis of tetanus).
Great, up to this point:
"Action Potential Produced
"The muscle fiber is now receiving Na+, which makes the inside of the muscle fiber more positively charged. This triggers a muscle action potential, which leads to a contraction of the muscle fiber; a more positively charged or depolarized muscle fiber forms the basis of how muscles contract."
So side A of the muscle is more positively charged than side B, which causes side A of the muscle to ... (shorten, lengthen, twitch?) because ... (?) By Anonymous on 19-08-12 at 04:38pm