MUSCARINE RECEPTORS REGULATING ELECTRICALLY-EVOKED RELEASE OF ACETYLCHOLINE IN HIPPOCAMPUS ARE LINKED TO PERTUSSIS-TOXIN-SENSITIVE G-PROTEINS BUT NOT TO ADENYLATE-CYCLASE

[H-3]Acetylcholine release elicited with 360 pulses/3 Hz from slices of rabbit hippocampus is facilitated in the presence of the muscarine (M) receptor antagonist atropine (indicating the existence of autoinhibition) and diminished by the M receptor agonists carbachol and oxotremorine. N-Ethylmaleimide (30 muM) and pertussis toxin (8 ug/ml) counteracted antagonist-induced facilitation and agonist-induced inhibition of release, suggesting that a pertussis toxin-sensitive GTP-binding protein is involved in the chain of events mediating activation of M receptors to inhibition of release. Neither 8-bromo-cyclic AMP (300 muM), a membrane analogue of cyclic AMP, nor rolipram (10 muM), a phosphodiesterase inhibitor, affected electrically evoked release of [H-3]acetylcholine. They also did not influence the oxotremorine-induced inhibition of transmitter release. In conclusion, no evidence was found for the assumption that activation of M autoreceptors is linked to inhibition of adenylate cyclase.