EFFECTS OF MUSCIMOL INACTIVATION OF THE CEREBELLAR INTERPOSED-DENTATENUCLEAR-COMPLEX ON THE PERFORMANCE OF THE NICTITATING-MEMBRANE RESPONSE IN THE RABBIT

Citation
V. Bracha et al., EFFECTS OF MUSCIMOL INACTIVATION OF THE CEREBELLAR INTERPOSED-DENTATENUCLEAR-COMPLEX ON THE PERFORMANCE OF THE NICTITATING-MEMBRANE RESPONSE IN THE RABBIT, Experimental Brain Research, 100(3), 1994, pp. 453-468
Citations number
70
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00144819
Volume
100
Issue
3
Year of publication
1994
Pages
453 - 468
Database
ISI
SICI code
0014-4819(1994)100:3<453:EOMIOT>2.0.ZU;2-W
Abstract
Intracranial microinjections of the GABA, agonist muscimol were used t o assess the involvement of the dentato-interposed cerebellar nuclear complex in the performance of the conditioned (CR) and unconditioned ( UR) nictitating membrane responses in the rabbit. Specifically, the ex periments test the hypothesis that the cerebellar nuclei are involved in the performance of both the CRs and URs. The experiments employed t emporary nuclear lesions to disrupt the CRs in order to examine parall el effects on URs. Animals were conditioned in a standard delay condit ioning paradigm. Injection sites at which the muscimol application dis rupted execution of the CRs were identified in each rabbit. Once these sites were found, the effects of muscimol and saline injections were evaluated while alternating paired trials with unpaired trials in whic h only the unconditioned stimuli were applied. There are two main find ings in the present study. First, the activation of the GABA, receptor s in the dentato-interposed cerebellar nuclear region reduced the ampl itude and increased the latency of the UR. This change in the UR close ly paralleled the disruption of the CR. This observation is consistent with the notion that the cerebellum is involved in the regulation of defensive flexion reflexes. Second, cerebellar nuclear inactivation di d not eliminate the tone-induced enhancement of the UR. This finding s uggests the presence of cerebellum-independent circuits subserving the intermodal interaction between the conditioned and unconditioned stim uli.