Mc. Xi et al., DORSAL SPINOCEREBELLAR TRACT NEURONS ARE NOT SUBJECTED TO POSTSYNAPTIC INHIBITION DURING CARBACHOL-INDUCED MOTOR INHIBITION, Journal of neurophysiology, 78(1), 1997, pp. 137-144
Dorsal spinocerebellar tract (DSCT) neurons in Clarke's column in the
lumbar spinal cord of cats anesthetized with alpha-chloralose were rec
orded intracellularly. The membrane potential activity and electrophys
iological properties of these neurons were examined before and during
the state of active-sleep-like motor inhibition induced by the injecti
on of carbachol into the nucleus pontis oralis. The synaptic activity
of DSCT neurons during carbachol-induced motor inhibition did not chan
ge compared with that during control conditions. In particular, there
was an absence of inhibitory postsynaptic potentials (IPSPs) in high-g
ain recordings from DSCT neurons and the resting membrane potential of
DSCT neurons was not significantly hyperpolarized during carbachol-in
duced motor inhibition. The mean amplitude of both monosynaptic excita
tory postsynaptic potentials and disynaptic IPSPs evoked in DSCT neuro
ns following stimulation of group I muscle afferents after the injecti
on of carbachol was similar to that evoked before the injection of car
bachol. There were no significant changes in the mean input resistance
and membrane time constant of DSCT neurons during carbachol-induced m
otor inhibition. We conclude that, in contrast to lumbar motoneurons,
DSCT neurons in Clarke's column are not postsynaptically inhibited dur
ing carbachol-induced motor inhibition. Therefore the population of sp
inal cord Ib interneurons that inhibit both DSCT neurons and lumbar mo
toneurons is not likely to be the interneurons that are responsible fo
r the postsynaptic inhibition of motoneurons that occurs during carbac
hol-induced motor inhibition. The present findings also indicate that
transmission through the DSCT is not modulated by postsynaptic inhibit
ion at the level of DSCT neurons during carbachol-induced motor inhibi
tion.