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The postural adjustments that accompany the limb flexion following stimulation of the motor cortex in the cat are in part at least mediated by the lateral vestibular nucleus (LVN). In fact, inactivation of vestibulospinal (VS) neurons by unilateral injection of GABA agonists into the LVN decreased the early component of the responses in all of the postural limbs without modifying the threshold, latency, or amplitude of the cortically induced flexion movement. Just the opposite result was obtained after injection into the same structure of GABA antagonists. Experiments were performed to find out whether these VS influences were somatotopically organized. Microinjection of 0.25 microL of the GABA-A agonist muscimol or the GABA-B agonist baclofen (at 1.5 to 4 micrograms/microL saline) into the rostroventral part of the LVN (rvLVN) of one side produced hypotonia in the ipsilateral and hypertonia in the contralateral forelimb. The same injection also reduced the early component of the postural responses to cortical stimulation in both forelimbs, but not in the hindlimbs. On the other hand, unilateral injection of the same agents into the dorsocaudal part of the LVN (dcLVN) produced similar effects, but they were limited to the hindlimbs. The results obtained, which lasted for about 2 to 3 h, were not only site-specific but were also dose-dependent. Injection into the rvLVN or dcLVN of 0.25 microL of the GABA-A antagonist bicuculline or the GABA-B antagonist phaclofen (at 8 or 5 micrograms/microL saline) produced localized changes in posture as well as in the post-urokinetic responses to cortical stimulation. These were opposite in sign to those elicited by the corresponding agonists. In conclusion, it appears that: 1) the motor cortex utilizes descending volleys passing through the LVN in order to elicit the early postural adjustments during a cortically induced limb movement; 2) the resulting VS influences are somatotopically organized; 3) the amplitude of these postural responses can be affected by inhibitory influences probably exerted by Purkinje cells of the cerebellar vermis on the related VS neurons through both GABA-A and GABA-B receptors.

International audience; The early component of the postural responses which accompany the limb flexion during unilateral stimulation of the motor cortex in the cat is not of reflex origin, but results from a central command. These postural adjustments are characterized by a decreased force under the limb diagonally opposite to the moving one and an increased force under the other two. Since the lateral vestibular nucleus (LVN) exerts an excitatory influence on ipsilateral limb extensor motoneurons, experiments were performed in cats to establish whether the cortical-induced postural changes were mediated through the LVN. This structure is tonically inhibited by GABAergic synapses originating from Purkinje cells of the cerebellar vermis, so that local microinjection into the LVN of GABA agonists or antagonists should either decrease or increase the spontaneous discharge of their neurons. Unilateral microinjection of 0.25 microliters of the GABA-A agonist muscimol or the GABA-B agonist baclofen (at 2-4 micrograms/microliters saline) into the LVN produced a short-lasting episode of ipsilateral postural hypotonia and contralateral hypertonia, during which the cats were unable to stand on the measurement platform. When, shortly after, some recovery of the postural activity appeared, no changes in threshold, latency or amplitude of the cortical-induced flexion movement were observed; however, the early component of the postural responses decreased in the other three limbs. Moreover, the slope of the response curve of the moving limb remained unmodified, while that of the early component of the postural responses, which involved the remaining limbs, decreased following stimulation of the motor cortex at different stimulus intensities. These effects started a few min after the injection and lasted for about 2-3 h. The effects described above were dose-dependent. Moreover, histological controls indicated that the structure responsible for these postural changes corresponded to the middle part of the LVN. The specificity of the results was shown by the fact that unilateral microinjection of 0.25 microliters of the GABA-A antagonist bicuculline or the GABA-B antagonist phaclofen (at 5-8 micrograms/microliter saline) into the LVN produced a postural asymmetry opposite in sign to that elicited in the same experiments by the corresponding agonists. These injections did not modify the amplitude of the cortical-induced limb flexion, but rather enhanced the amplitude of the early component of the postural responses in the other three limbs.(ABSTRACT TRUNCATED AT 400 WORDS)