CONVULSIONS INDUCED BY ELECTRICAL STIMULATION OF THE BRAINSTEM IN RATS
Abstract number :
2.065
Submission category :
Year :
2005
Submission ID :
5369
Source :
www.aesnet.org
Presentation date :
12/3/2005 12:00:00 AM
Published date :
Dec 2, 2005, 06:00 AM
Authors :
1Ann Lam, and 2Michael E. Corcoran
Previous studies have examined the susceptibility of brainstem sites to kindling, but the results have been conflicting. Some researchers have reported that afterdischarge (AD) and conventional kindling occur with stimulation of the brainstem (e.g., deep mesencephalic nucleus of reticular formation, periaqueductal gray) in rats, whereas others have described convulsions without AD (e.g., mesencephalic reticular formation). Furthermore, it has been reported that kindling of brainstem sites results in transfer to kindling of forebrain sites. In an attempt to resolve the discrepancies, we re-examined the convulsive responses of brainstem sites to kindling stimulation. Male Long-Evans hooded rats received 1-sec trains of balanced square wave stimulation, at 60 pulse pairs/sec, in various brainstem sites. EEG was recorded from the stimulated site and from another electrode in anterior neocortex. Thresholds for AD or convulsive responses were measured, and convulsive responses were scored. Stimulation was applied once daily for at least 5 days. We failed to observe AD after stimulation of the nucleus reticularis pontis oralis (RPO), periaqueductal gray (PAG), or lateral dorsal tegmental nucleus (LDTg). However, stimulation at sufficient intensities ([gt]1000 [mu]A) triggered convulsive responses that occurred after termination of stimulation. Convulsions triggered by stimulation of RPO comprised tonic retraction and extension of the forelimbs and hindlimbs, resembling the response to maximal electroconvulsive shock, without clonic signs. Convulsions triggered by stimulation of PAG or LDTg comprised both tonic and clonic movements, often with hindlimb retraction but no extension. There were no obvious changes in the convulsive responses to subsequent stimulations. Our results indicate that components of intense convulsions can be triggered by short trains of electrical stimulation applied to sites in the brainstem. The convulsions occur in the absence of epileptiform AD in either the brainstem or anterior neocortex. The convulsive responses to extended stimulation of the brainstem (i.e., [gt]5 stimulations), potential interactions with kindling from forebrain sites, and possible triggering of AD in limbic sites such as amygadla or hippocampus remain to be investigated. (Supported by NSERC and CIHR.)