Abstracts

Electroconvulsive Shock Is Not an Adequate Stimulus to Cause the Formation of Hilar Basal Dendrites on Dentate Granule Cells.

Abstract number : 1.086
Submission category :
Year : 2000
Submission ID : 2388
Source : www.aesnet.org
Presentation date : 12/2/2000 12:00:00 AM
Published date : Dec 1, 2000, 06:00 AM

Authors :
Charles E Ribak, Trinh T Dinh, Peter H Tran, UC Irvine, Irvine, CA.

Rationale: Previous studies showed that hippocampal dentate granule cells with hilar basal dendrites (HBDs) are found in the brains of epileptic adult rats. HBDs are postsynaptic to mossy fiber axons, thus interconnecting granule cells, and may contribute to the hyperexcitability of hippocampal circuits in epilepsy. Temporal lobe epilepsy with status epilepticus is an adequate stimulus for hilar basal dendrite formation. The present study determined whether a single seizure may cause the formation of hilar basal dendrites. Methods: Electroconvulsive shock (ECS) was administered to rats and produced tonic-clonic motor seizures for 20 sec. Brains were analyzed at weekly intervals from 1-4 weeks following the last ECS from rats with a single ECS and those with 4 ECSs. Granule cells were visualized in either retrograde biocytin preparations or with the Golgi method. Rats with pilocarpine-induced seizures were a positive control and untreated rats were a negative control. Results: Rats with single or multiple ECS treatments did not display HBDs in either biocytin or Golgi preparations at any of the timepoints examined. The morphology of granule cells in these preparations was normal. In contrast, many granule cells from pilocarpine-treated rats had HBDs in agreement with previous studies from this laboratory. The untreated rats did not show any granule cells with HBDs. Conclusions: The results of this study indicate that a single seizure is not an adequate stimulus for the formation of HBDs on dentate granule cells. Previous studies with pilocarpine-, kainate- or perforant path stimulation-induced epilepsy that showed the presence of HBDs on granule cells have associated hilar neuronal loss. The lack of neuronal death following ECS suggests that hilar damage may be essential for HBD formation. [Supported by NIH grant NS-38331]