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Effect of Complete and Partial Bilateral Lesions of the Deep Cerebellar Nuclei on Amygdaloid Kindling in Rats
Author(s) -
Min Jason K.,
Valentine Pamela A.,
Teskey G. Campbell
Publication year - 1998
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1998.tb01153.x
Subject(s) - clonus , epileptogenesis , kindling , dentate nucleus , fastigial nucleus , neuroscience , amygdala , cerebellum , lesion , forelimb , tonic (physiology) , medicine , epilepsy , psychology , pathology
Summary:Purpose: The roles of the deep cerebellar nuclei in epileptogenesis and seizure expression are not well defined. To determine their properties, we examined the effects of lesions to the dentate, fastigial, and interpositus nuclei in adult rats that were electrically kindled in the amygdaloid complex. Changes in afterdischarge duration (ADD) as well as the expression and progression of behavioral seizures to fully generalized tonic‐clonic convulsions (stage 5) were assessed. Methods: Fifty rats first underwent bilateral electrolytic lesions of either the dentate, fastigial, or interpositus nuclei. After a 7–day recovery period, they were kindled daily until they manifested two stage 5 convulsions. Careful histological examination was used to determine lesion extent. Results: When the dentate or fastigial nucleus was completely destroyed on the side contralateral to the stimulated amygdala, fewer stimulations were required to produce stage 5 seizures and latencies to the expression of forelimb clonus were shorter, as were ADD. On the other hand, when the dentate or fastigial neucleus was only partly obliterated on the contralateral side, more stimulations were required to produce stage 5 seizures and ADD was longer. Neither complete nor partial 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 retard epileptogenesis and inhibit clonic behaviors, but paradoxically may facilitate ADD.