Serotonin-induced depolarization of rat facial motoneurons in vivo: comparison with amino acid transmitters.

Intracellular recordings were obtained from facial motoneurons in anesthetized rats. The effects of iontophoretically applied serotonin were compared to those of the excitatory amino acids glutamate and DL-homocysteic acid (DLH), and the inhibitory amino acids, glycine, GABA and muscimol, under various conditions of membrane polarization and intracellular chloride concentration. Iontophortically applied serotonin caused a depolarization of facial motoneurons which was accompanied by increased input resistance and increased neuronal excitability. Experiments comparing the response to serotonin with those of glycine, GABA, and muscimol demonstrated that the serotonin effect does not involve changes in membrane conductance to chloride. Comparisons of serotonin with glutamate and DLH at varying levels of membrane hyperpolarization indicated that the serotonin-induced depolarization is not caused by increased conductance to sodium or calcium, and differs in its underlying ionic mechanism from depolarizations induced by glutamate and DLH. Results were consistent with the hypothesis that serotonin causes depolarization, increased input resistance, and increased excitability in rat facial motoneurons by decreasing resting membrane conductance to potassium ions. Such changes in motoneurons in the brain stem and spinal cord probably account for some of the physiological and behavioral effects observed during pharmacological activation of serotonin receptors.