Both Presynaptic Nicotinic-like and Muscarinic-like Autoreceptors Regulate Acetylcholine Release at an Identified Neuro-neuronal Synapse of Aplysia
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The possible involvement of cholinergic presynaptic receptors regulating evoked quantal acetylcholine (ACh) release was investigated at an identified cholinergic neuro-neuronal synapse in the buccal ganglion of Aplysia, using cholinergic agonists (carbachol, pilocarpine, oxotremorine) and/or antagonists (curare, atropine, hexamethonium). Bath applied carbachol or pilocarpine (10(-8) M to 10(-4) M) induced a decrease in the evoked quantal release of ACh. As the effects of carbachol were prevented by atropine (5.10(-6) M) and not by curare (10(-5) M), it was concluded that carbachol activated presynaptic muscarinic-like receptors implicated in a negative feed-back on ACh release. On the contrary, oxotremorine (up to 10(-4) M) induced a potentiation of ACh release which was suppressed by curare (4.10(-6) M) or hexamethonium (10(-5) M) but not by atropine (5.10(-6) M) pointing to the activation of presynaptic nicotinic-like receptors implicated in a positive feed-back on ACh release. Moreover, in the presence of curare, oxotremorine decreased ACh release: this suggested that oxotremorine also activated the presynaptic muscarinic-like receptors. These results revealed the conjoint presence, on the same terminal, of both muscarinic-like and nicotinic-like autoreceptors.
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