acetylcholine is released from the neuromuscular junction to stimulate muscle contraction.
where is acetylcholine released from to stimulate muscle contraction?
the neuromuscular junction
nicotinic acetylcholine receptors, or nachrs, are receptor polypeptides that respond to the neurotransmitter acetylcholine. nicotinic receptors also respond to drugs as the agonist nicotine. they are found in the central and peripheral nervous system, muscle, and many other tissues of many organisms. at the neuromuscular junction they are the primary receptor in muscle for motor nerve-muscle communication that controls muscle contraction. in the peripheral nervous system: (1) they transmit outgoing signals from the presynaptic to the postsynaptic cells within the sympathetic and parasympathetic nervous system, and (2) they are the receptors found on skeletal muscle that receive acetylcholine released to signal for muscular contraction. in the immune system, nachrs regulate inflammatory processes and signal through distinct intracellular pathways. in insects, the cholinergic system is limited to the central nervous system.
nicotinic acetylcholine receptor
the muscle contraction of a ballistic muscle movement can exhibit a muscle coactivation of concurrent agonist and antagonist muscles or the characteristic triphasic agonist/antagonist/agonist muscle activation. electromyography (emg) recordings of demonstrate the triphasic muscle activation begins with a brief agonist motor unit activation signal with firing rates of 60 to 120 hz that may last for 100ms and occurs 50 to 100ms before movement begins. the firing rates of ballistic movements are much higher than that of slow ramp movements (5–15 hz). the brief agonist muscle contraction is thus followed by antagonist muscle unit activation. the degree of antagonist muscle unit activation is dependent on the task at hand unlike the first agonist muscle activation which is independent to environmental stimuli. the function of the antagonist muscle contraction is believed to control the amplitude and timing of ballistic movements. antagonist muscle contraction may serve to prevent injury to joints by preventing the limb from overextending itself and also function to control the distance and time the limb is being moved. experiments involving ballistic movement of small amplitudes show a marked increase in antagonist muscle activation and experiments where distance moved is not controlled antagonist muscle activation was decreased or absent. the second agonist muscle activation is suggested to terminate the negative acceleration of the antagonist muscle contraction and thus the ballistic movement.
ballistic movement