Intracellular studies showing modulation of facial motoneurone excitability by serotonin

Abstract

The application of serotonin to certain myenteric plexus neurons in the guinea pig small intestine causes a slow depolarization of membrane potential, accompanied by increased neuronal excitability and input resistance. Microiontophoretic application of large amounts of serotonin onto mammalian spinal motoneurons is reported to cause membrane hyperpolarization and decreased excitability. Based on recording spinal reflex activity, serotonin was reported to enhance net motoneuron activity. Moreover, studies using extracellular single-cell recording techniques indicate that serotonin in small amounts facilitates synaptically or glutamate-induced excitation of mammalian motoneurons in the facial nucleus and spinal cord. These facilitatory actions were modulatory in nature, as serotonin did not induce motoneuron spiking in the absence of extrinsic excitatory input. The membrane mechanisms underlying these modulatory effects were investigated by obtaining intracellular recordings from rat facial motoneurons during extracellular microiontophoretic application of serotonin, methysergide (a serotonin antagonist) and noradrenaline [norepinephrine, NE]. Serotonin caused a slow depolarization of membrane potential of .apprx. 5 mV which remained subthreshold, accompanied by an increase in electrical excitability of the neuron, and an increase in input resistance. NE caused the same changes. Methysergide antagonized the effects of serotonin, but not NE; these actions of serotonin are selective and receptor mediated.