The primary amino acid structure of each subtype has 460~590 amino acid residues. The mechanism of action is coupling with G protein, activating phospholipase C and M receptors, inhibiting adenylate cyclase, activating K+ channels or inhibiting Ca2+ channels. N receptors can be divided into two subtypes.
The receptor on the postsynaptic membrane of ganglion neurons and the central N receptor are N 1 receptor, and quaternary ammonium hexadecane is a blocking agent. The receptor on the membrane of skeletal muscle endplate is N2 receptor, and quaternary ammonium decahydrate is a blocking agent. Turmeric is an isotype blocker of N 1 and N2.
N-type cholinergic receptors are composed of four subunits (α, β, γ, δ
)5-mer。 These subunits are attracted to each other and wrapped into a channel structure, and the two α subunits are the binding sites of acetylcholine. When acetylcholine and α -subunit can open ion channels, the flow rates of Na+, Ca2+ and K+ can be adjusted. When the action potential reaches the motor nerve endings, the presynaptic membrane depolarizes, leading to the outflow of cell cracks, releasing acetylcholine to combine with the N receptor of neuromuscular junction, resulting in local depolarization potential, namely endplate potential. When the endplate potential exceeds the diffusion depolarization threshold of muscle fibers, the voltage-gated ion channels on the membrane can be opened. At this time, a large number of Na+ and Ca2+ enter the cell, producing action potential, which leads to muscle contraction.