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 potential is not yet fully proven. 6. It can be concluded that the excitatory and inhibitory synaptic effects evoked in the buccal neurones by the stimulation of the 5‐HT‐containing‐giant cerebral neurones are very likely mediated by 5‐HT.