POSTINHIBITORY REBOUND DURING LOCOMOTOR-LIKE ACTIVITY IN NEONATAL RAT
MOTONEURONS IN VITRO.
Sandrine BERTRAND, Jean-Ren‚ CAZALETS.
CNRS, NBM, 31 chemin Joseph Aiguier, BP 71, 13402 Marseille CEDEX 20
France.
APStracts 4:0253N, 1997.
ABSTRACT
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 which 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 which 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 were still rhythmically depolarized). 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.
Received 17 April 1997; accepted in final form 10 September 1997.
APS Manuscript Number J309-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 7 October 1997