Abstract
Intracellular recordings were made from neurons of rabbit vesical pelvic (parasympathetic) ganglia (VPG). Application of 5-hydroxytryptamine (5-HT, 0.3–30 μM) produced an initial depression followed by a long-lasting facilitation of the fast excitatory postsynaptic potential (e.p.s.p.) evoked by stimulation of the pelvic preganglionic nerve. The facilitation of nicotinic transmission lasted for 30–120 min, even when 5-HT was removed from the superfusing solution. 5-HT (0.3–30 μM) did not change the depolarization induced by a direct application of acetylcholine (ACh) to the VPG neurons pretreated with 1 μM atropine. 5-HT also caused an initial depression followed by an increase in the quantal content of the fast e.p.s.p. It is, therefore, suggested that diphasic effect of 5-HT on the nicotinic transmission is due mainly to a modulation of the ACh-release from presynaptic nerve terminals. Methysergide (5 μM), mianserin (5–30 μM) and ICS 205–930 (100–300 nM) did not antagonize the presynaptic actions of 5-HT on the nicotinic transmission, suggesting that the presynaptic 5-HT receptor may belong to a class of 5-HT 1 subtypes. Spiperone (1 μM), a selective 5-HT 1A antagonist, blocked the 5-HT-induced inhibition of the fast e.p.s.p. Under the effect of spiperone, the facilitation appeared soon after application of 5-HT. The facilitation of the fast e.p.s.p. may be mediated through a 5-HT 1B or 5-HT 1C subtype. Lowering temperature of the external solution eliminated the 5-HT-induced facilitation of the nicotinic transmission. Forskolin produced a presynaptic facilitation of the fast e.p.s.p., without producing an initial depression. 3-Isobutyl-1-methylxanthine (10 μM) potentiated the facilitatory action of 5-HT. Bath-application of dibutyryl cyclic adenosine monophosphate (cAMP) (1–6 mM) and 8-bromo-cyclic AMP (2–5 mM) mimicked the effect of 5-HT in producing the facilitation of the fast e.p.s.p.s. All data presented are consistent with the hypothesis that 5-HT, acting on presynaptic 5-HT 1 receptors, causes a facilitation in the release of ACh from preganglionic nerve terminals possibly mediated through an activation of adenylate cyclase.
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