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  • Title: Presynaptic actions of curare and atropine on quantal acetylcholine release at a central synapse of Aplysia.
    Author: Baux G, Tauc L.
    Journal: J Physiol; 1987 Jul; 388():665-80. PubMed ID: 3656203.
    Abstract:
    1. In a cholinergic synaptic couple in the buccal ganglion of Aplysia california, where the synaptic areas are situated close to the somata (500 micron), we were able to control transmitter release by stimulating the cell body of the presynaptic neurone with long depolarizing pulses in the presence of tetrodotoxin (TTX). 2. Statistical analysis of noise occurring at the peak of the long-depolarization-induced post-synaptic current (p.s.c.) responses allowed us to calculate the amplitude and the decay time of the miniature post-synaptic currents (m.p.s.c.s). These data were used to calculate the quantal content of the responses. 3. Bath-applied tubocurarine reduced the amplitude of the long-depolarization-induced p.s.c. more than that of the m.p.s.c.s, indicating that tubocurarine exerts a depressive presynaptic action on the quantal content of the post-synaptic responses. 4. Tubocurarine injected into the presynaptic neurone blocked synaptic transmission without decreasing the size of the m.p.s.c.s probably by acting on the mechanism of transmitter release. 5. Bath-applied atropine (10(-6) and 10(-5) M) caused a slight decrease of the m.p.s.c.s but the long-depolarization-induced p.s.c.s increased, as did the quantal content. Higher concentrations of atropine depressed strongly both the m.p.s.c. and the quantal content. 6. Injection of atropine into the presynaptic neurone had the same effect as its bath application, probably due to the leakage of the drug into the synaptic cleft; the effect depended on the concentration reached in the cleft, i.e. on the quantity of injected drug. The synapses of the neighbouring cholinergic neurone were also affected by this leak of atropine. 7. The presence of nicotinic presynaptic receptors blocked by tubocurarine, and muscarinic presynaptic receptors blocked by atropine, which regulate synaptic transmission by facilitating and depressing the ACh release respectively, is discussed.
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