[Synaptic effects of nicotinic and muscarinic agonists in the sympathetic ganglia of the frog].

Superfusion of isolated frog sympathetic ganglia with nicotinic agonists (suberyldicholine, tetramethylammonium, DMPP), as well as with acetylcholine in the presence of atropine, caused short-term depolarization of a single ganglion cell and blockade of synaptic transmission. Muscarinic agonists (methylfurmethide, methyl dilvasen, acetylcholine) caused sustained depolarization which was not accompanied by transmission failure. Oxotremorine did not change membrane potential at concentrations up to 1.10(-5) mol/l, but at a lower concentration (1.10(-6) mol/l) it produced about a two-fold decrease of EPSP quantum content. This allows the presynaptic muscarinic receptors to be related to M2 type. Inhibition of acetylcholinesterase markedly potentiated postsynaptic effect of methylfurmethide; as a result, there was a shift of the dose-response curve to the lower concentrations of agonist. The postsynaptic muscarinic receptors were found to have high stereoselectivity that was seen in the case of enantiomers of methyl dilvasen (F-2268). The obtained results elucidate changes in the ganglionic transmission, the transmitter being present in the synaptic cleft.