Intracellular studies showing modulation of facial motoneurone excitability by serotonin.

The application of serotonin to certain myenteric plexus neurones in the guinea pig small intestine causes a slow depolarization of membrane potential, accompanied by increased neuronal excitability and input resistance. On the other hand, microiontophoretic application of large amounts of serotonin onto mammalian spinal motoneurones is reported to cause membrane hyperpolarization and decreased excitability. However, on the basis of recording spinal reflex activity, serotonin has been reported to enhance net motoneurone activity. Moreover, studies using extracellular single-cell recording techniques indicate that serotonin in small amounts facilitates synaptically or glutamate-induced excitation of mammalian motoneurones in the facial nucleus and spinal cord. It was suggested that these facilitatory actions were modulatory in nature, as serotonin did not induce motoneurone spiking in the absence of extrinsic excitatory input. The study reported here investigated the membrane mechanisms underlying these modulatory effects by obtaining intracellular recordings from rat facial motoneurones during extracellular microiontophoretic application of serotonin, methysergide (a serotonin antagonist) and noradrenaline. Serotonin caused a slow depolarization of membrane potential of about 5 mV which remained sub-threshold, accompanied by an increase in electrical excitability of the neurone, and an increase in input resistance. Noradrenaline caused the same changes. Methysergide antagonized the effects of serotonin, but not noradrenaline, indicating that these actions of serotonin are selective and receptor mediated.