EFFECT OF COMPLETE AND PARTIAL BILATERAL LESIONS OF THE DEEP CEREBELLAR NUCLEI ON AMYGDALOID KINDLING IN RATS

Citation
Jk. Min et al., EFFECT OF COMPLETE AND PARTIAL BILATERAL LESIONS OF THE DEEP CEREBELLAR NUCLEI ON AMYGDALOID KINDLING IN RATS, Epilepsia, 39(7), 1998, pp. 692-699
Citations number
38
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00139580
Volume
39
Issue
7
Year of publication
1998
Pages
692 - 699
Database
ISI
SICI code
0013-9580(1998)39:7<692:EOCAPB>2.0.ZU;2-P
Abstract
Purpose: The roles of the deep cerebellar nuclei in epileptogenesis an d seizure expression are not well defined. To determine their properti es, we examined the effects of lesions to the dentate, fastigial, and interpositus nuclei in adult rats that were electrically kindled in th e amygdaloid complex. Changes in afterdischarge duration (ADD) as well as the expression and progression of behavioral seizures to fully gen eralized tonic-clonic convulsions (stage 5) were assessed. Methods: Fi fty rats first underwent bilateral electrolytic lesions of either the dentate, fastigial, or interpositus nuclei. After a 7-day recovery per iod, they were kindled daily until they manifested two stage 5 convuls ions. Careful histological examination was used to determine lesion ex tent. Results: When the dentate or fastigial nucleus was completely de stroyed on the side contralateral to the stimulated amygdala, fewer st imulations were required to produce stage 5 seizures and latencies to the expression of forelimb clonus were shorter, as were ADD. On the ot her hand, when the dentate or fastigial neucleus was only partly oblit erated on the contralateral side, more stimulations were required to p roduce stage 5 seizures and ADD was longer. Neither complete nor parti al lesions of the interpositus nuclei had any effect on the number of stimulations to reach a stage 5 seizure, latency to the expression of clonus, or ADD. Conclusions: Our findings suggest that the dentate and fastigial nuclei, but not the interpositus nuclei, may normally retar d epileptogenesis and inhibit clonic behaviors, but paradoxically may facilitate.