Article date: September 1972
By: G. M. LEES, S. NISHI in Volume 46, Issue 1, pages 78-88
. Mechanisms of action of hexamethonium, mecamylamine and (+)‐tubocurarine on the rabbit superior cervical ganglion were investigated by intracellular recording techniques.
. In concentrations up to 1 mm, none of these drugs affected the resting membrane potential nor altered the excitability of the postganglionic neurone to direct or antidromic stimulation.
. Post‐tetanic potentiation of the excitatory postsynaptic potential (e.p.s.p.) was inhibited by mecamylamine (10–100 μm) but not affected by either hexamethonium (5–100 μm) or (+)‐tubocurarine (10–50 μm).
. The decline in amplitude of successive e.p.s.ps in a train (40 Hz) was not influenced by hexamethonium or (+)‐tubocurarine but was greatly exaggerated in the presence of mecamylamine; desensitization of the receptors for acetylcholine was excluded as a possible explanation for this latter finding.
. Mecamylamine depressed the quantal content of e.p.s.ps in a train, with the exception of the first e.p.s.p. which had an increased quantal content.
. Reduction in quantal content was attributed to a substantial fall in the size of the store of quanta of transmitter immediately available for release and to a reduction in the rate of mobilization of acetylcholine into that store; mecamylamine also caused a simultaneous increase in the fractional release.
. Hexamethonium and (+)‐tubocurarine had no effect on transmitter release.
. The time‐course of presynaptic effects of mecamylamine was similar to the duration of its postsynaptic blocking action.
. It is concluded that inhibition of ganglionic transmission by mecamylamine is due to both presynaptic and postsynaptic inhibitory actions; in contrast, hexamethonium and (+)‐tubocurarine reduce transmission solely by their postsynaptic actions.
. Mechanisms of action of hexamethonium, mecamylamine and (+)‐tubocurarine on the rabbit superior cervical ganglion were investigated by intracellular recording techniques.
. In concentrations up to 1 mm, none of these drugs affected the resting membrane potential nor altered the excitability of the postganglionic neurone to direct or antidromic stimulation.
. Post‐tetanic potentiation of the excitatory postsynaptic potential (e.p.s.p.) was inhibited by mecamylamine (10–100 μm) but not affected by either hexamethonium (5–100 μm) or (+)‐tubocurarine (10–50 μm).
. The decline in amplitude of successive e.p.s.ps in a train (40 Hz) was not influenced by hexamethonium or (+)‐tubocurarine but was greatly exaggerated in the presence of mecamylamine; desensitization of the receptors for acetylcholine was excluded as a possible explanation for this latter finding.
. Mecamylamine depressed the quantal content of e.p.s.ps in a train, with the exception of the first e.p.s.p. which had an increased quantal content.
. Reduction in quantal content was attributed to a substantial fall in the size of the store of quanta of transmitter immediately available for release and to a reduction in the rate of mobilization of acetylcholine into that store; mecamylamine also caused a simultaneous increase in the fractional release.
. Hexamethonium and (+)‐tubocurarine had no effect on transmitter release.
. The time‐course of presynaptic effects of mecamylamine was similar to the duration of its postsynaptic blocking action.
. It is concluded that inhibition of ganglionic transmission by mecamylamine is due to both presynaptic and postsynaptic inhibitory actions; in contrast, hexamethonium and (+)‐tubocurarine reduce transmission solely by their postsynaptic actions.
DOI: 10.1111/j.1476-5381.1972.tb06850.x
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