Postinhibitory rebound during locomotor-like activity in neonatal rat motoneurons in vitro.

The aim of this study was to establish how a membrane property contributes to the neuronal discharge during ongoing behavior. We therefore studied the role of the postinhibitory rebound (PIR) in the bursting discharge of lumbar motoneurons intracellularly recorded in newborn rat in vitro brain stem/spinal cord preparation. The PIR is a transient depolarization that occurs after a hyperpolarization. We first investigated how it was expressed during experimentally induced hyperpolarizations. Its amplitude increased with the inhibition and was voltage dependent. The Ca2+ channel blockers Mn2+ and Co2+ partly suppressed the PIR in a few of the motoneurons tested. When hyperpolarized, the motoneurons exhibited a sag that was associated with the PIR. Adding caesium to the bath abolished both sag and rebound, which suggested that the PIR in the lumbar motoneurons was mainly due to the activation of the inward rectifying current IQ. In the second part, we studied the physiological involvement of PIR during fictive locomotion induced by bath application of N-methyl-D-L-aspartate and serotonin. We established that experimentally induced PIR could initiate or modulate the bursting discharge of motoneurons during fictive locomotion. We then studied whether the firing patterns of the motoneurons were correlated in one way with the synaptic inhibition. When the monosynaptic inhibitory input to the motoneurons was abolished with the glycinergic blocker strychnine, these neurons stopped discharging (although they still were depolarized rhythmically). The firing of action potentials was restored by applying negative current pulses. This study provides evidence as to how one membrane property in mammals is involved in a complex type of behavior, namely locomotion.