Presynaptic function modified by acetylcholine-receptor interaction in experimental autoimmune myasthenia gravis.
Rats with experimental autoimmune myasthenia gravis (EAMG) were studied to test if the postsynaptic receptor disease would be modified by a compensating presynaptic effect of acetylcholine (ACh) being mediated through the presynaptic receptor. In normal rat phrenic-diaphragms, the ACh quantum content was estimated using the cut-muscle technique by which the evoked release of transmitter can be measured in the absence of blocking agents; values were significantly increased when the ACh receptor was blocked by d-tubocurarine. In rats with EAMG, this presynaptic autoregulation acted to compensate the postsynaptic failure, but did not reach the range of d-tubocurarine-treated controls. Results may be explained by either the difference between the receptor sites for myasthenic antibodies and d-tubocurarine or the immunological property of the presynaptic receptor which may differ from the postsynaptic one.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D001327:Autoimmune Diseases / Q000503:physiopathology*; D003964:Diaphragm / Q000294:innervation; D005260:Female; D008564:Membrane Potentials / Q000187:drug effects; D009045:Motor Endplate / Q000503:physiopathology; D009046:Motor Neurons / Q000502:physiology; D009157:Myasthenia Gravis / Q000503:physiopathology*; D009469:Neuromuscular Junction / Q000503:physiopathology; D010791:Phrenic Nerve / Q000503:physiopathology; D051381:Rats; D011917:Rats, Inbred Lew; D011950:Receptors, Cholinergic / Q000502:physiology*; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects; D014403:Tubocurarine / Q000494:pharmacology
D011950:Receptors, Cholinergic; D000109:Acetylcholine; D014403:Tubocurarine