Modulation of the sensitivity of nicotinic receptors in autonomic ganglia.
This article reviews some of the evidence suggesting that a variety of endogenous substances either facilitates or inhibits the sensitivity of nicotinic acetylcholine (ACh) receptors at the subsynaptic membrane of cholinergic synapses. It is noteworthy that 5-hydroxytryptamine and histamine act as competitive antagonists, like curare, presumably changing the affinity of ACh for the specific binding site on the nicotinic receptor. Catecholamine, neuropeptides, prostaglandin and glucocorticoids act as non-competitive antagonists on an allosteric site on the receptor-ionic channel complex. ATP and LH-RH (in a subpopulation of sympathetic neurons) caused a facilitation of the sensitivity of nicotinic receptors. The mode of actions of endogenous substances which modulate the nicotinic receptor-sensitivity is similar to those of pharmacological agents. Therefore, these neurotransmitters and neurohormones have been termed endogenous 'antagonists' or 'sensitizers'.
Akasu
T
T
Department of Physiology, Kurume University School of Medicine, Japan.
Tokimasa
T
T
D000109:Acetylcholine / Q000502:physiology; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D005725:Ganglia, Autonomic / Q000187:drug effects / Q000502:physiology*; D007700:Kinetics; D008959:Models, Neurological; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000502:physiology*; D012701:Serotonin / Q000494:pharmacology*
D011978:Receptors, Nicotinic; D012701:Serotonin; D000255:Adenosine Triphosphate; D000109:Acetylcholine