Sarcolema receptors
acetylcholine as far as i know is a neurotransmitter that ativates the mscle cells.
Organopesticides will increase the severity of muscle contraction beyond normal conditions. Acetylcholine esterase inhibition will allow a more than normal amount of acetylcholine to bind to receptors.
The neurotransmitter acetylcholine is released into the synaptic cleft to bind with receptors on muscle cells. Upon binding, the muscle cells contract.
It blocks the nicotinic cholinergic receptors on the muscle that normally bind the acetylcholine released by the motor neuron.
Once a triad has been achieved, Calcium ions get released. Once they're released they bind to troponin, which helps begin muscle contraction.
Acetylcholine is released at the neuromuscular junction and binds to a nicotinic receptor, causing an action potential to fire down the T tubules. The voltage change from this is sensed by the Sarcoplasmic Reticulum which then releases Ca2+ ions into the cytosol. The Ca2+ ions bind to troponin which moves tropomyosin from the active sites of the actin filament. Once the active sites are revealed, myosin quickly forms a cross bridge and begins contraction.
The presence of an enzyme called acetylcholinesterasethat degrades acetylcholine is what prevents an accumulation of the neurotransmitter and sustained muscle contraction. Acetylcholinesterase is an enzyme that can be found within the neuromuscular junction. Thus, when a nerve impulse causes the release of acetylcholine at the neuromuscular junction, there is a critical time in which the neurotransmitter can bind to receptors on the muscle before it is degraded.
They bind to regulatory sites on troponin to remove contraction inhibition
Muscle contraction results
Acetylcholine.
Calcium binds to the messenger protein Calmodulin. The calcium-calmodulin complex then activates myosin light chain kinase (MLCK), which phosphorylates myosin to allow it to bind to actin - producing contraction.
Calcium ions bind to troponin, changing troponin's shape