On the transmitter function of 5-hydroxytryptamine at excitatory and inhibitory monosynaptic junctions

1. Two symmetrical giant neurones located in the cerebral ganglion of Aplysia californica contain 4-6 p-mole 5-hydroxytryptamine (5-HT) and are able to synthesize it (Weinreich, McCaman, McCaman & Vaughn, 1973; Eisenstadt, Goldman, Kandel, Koike, Koester & Schwartz, 1973). Stimulation of each of these neurones evokes excitatory and inhibitory potentials in various cells of the ipsilateral buccal ganglion. In nine buccal neurones it evokes excitatory potentials, in other three, `classical' inhibitory potentials and in one neurone an `atypical' inhibitory potential. 2. The connexion between the giant cerebral neurone and the cells receiving either an excitatory or a `classical' inhibitory input from it are monosynaptic. TEA injection into the cerebral giant neurone, which prolongs the presynaptic spike, causes a gradual increase of both the excitatory and the inhibitory potentials. On the other hand, high Ca 2+ media, which block polysynaptic pathways, do not suppress these synaptic potentials. 3. The iontophoretic application of 5-HT to the buccal neurones receiving excitatory input from the giant cerebral neurones evokes depolarizations showing the pharmacological properties of both A - and A ′-responses to 5-HT (see preceding paper). Antagonists which block only the A -receptors (curare, 7-methyltryptamine, LSD 25) block partially the synaptic depolarizing potentials. Bufotenine, which blocks both the A - and A ′-receptors, completely blocks the excitatory potentials. Thus, the post-synaptic membrane of these buccal neurones appears to be endowed with both A - and A ′-receptors to 5-HT. 4. The `classical' inhibitory potentials elicited in three buccal neurones are hyperpolarizations which reverse at — 80 mV and are due to an increase in K + -conductance. The iontophoretic application of 5-HT to these post-synaptic neurones evokes hyperpolarizing B -responses which are also generated by an increase in K + -conductance. Antagonists which block the B -responses (bufotenine, methoxygramine) also block the inhibitory potentials. 5. The `atypical' inhibitory potential evoked in one buccal neurone consists in an hyperpolarization which increases in amplitude with cell hyperpolarization. Iontophoretic application of 5-HT to this buccal cell evokes an hyperpolarizing β-response which also increases in amplitude with cell polarization and results from a decrease in both Na + - and K + - conductances. The monosynaptic character of the `atypical' inhibitory