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 beta-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.
D000200:Action Potentials; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D002027:Bufotenin / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D003470:Culture Media; D003472:Curare / Q000494:pharmacology; D004123:Dimethylamines / Q000494:pharmacology; D066298:In Vitro Techniques; D007211:Indoles / Q000494:pharmacology; D007478:Iontophoresis; D008564:Membrane Potentials / Q000187:drug effects; D008738:Methyl Ethers / Q000494:pharmacology; D008974:Mollusca; D009474:Neurons / Q000502:physiology; D011188:Potassium / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology*; D012964:Sodium / Q000494:pharmacology; D013569:Synapses / Q000502:physiology*; D013570:Synaptic Membranes / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects*; D014363:Tryptamines / Q000494:pharmacology
D000319:Adrenergic beta-Antagonists; D003470:Culture Media; D004123:Dimethylamines; D007211:Indoles; D008738:Methyl Ethers; D014363:Tryptamines; D002027:Bufotenin; D012701:Serotonin; D003472:Curare; D012964:Sodium; D011188:Potassium; D002118:Calcium