Serotonin depolarizes cat spinal motoneurons in situ and decreases motoneuron afterhyperpolarizing potentials

Abstract

Mechanisms by which serotonin produces a long duration facilitation of spinal motoneuron excitability were investigated in decerebrate cats using intracellular recording combined with extracellular microiontophoresis. Serotonin was found to produce a slowly developing, small amplitude, long duration depolarization of the spinal motoneurons. This finding conflicts with early reports of serotonin-induced rapid hyperpolarization of cat spinal motoneurons, but exactly corresponds to more recent findings in rat facial motoneurons. The depolarization was accompanied by an increase in motoneuron excitability and an increase in membrane input resistance. In addition, serotonin reduced the motoneuron postspike afterhyperpolarizing potential in several motoneurons even though depolarization consistently occurred.