Intradentate colchicine retards the development of amygdala kindling.

Published

Journal Article

The mechanisms underlying the kindling model of epilepsy are unknown. Presumably, an altered network of neural circuits underlie amygdala kindling. Biochemical and radiohistochemical studies have pointed to the dentate granule cells (DGC) of the hippocampal formation as a member of this altered circuit. To test the role of these cells, colchicine, a neurotoxin of DGC, was directly injected into the dentate gyrus. Prior destruction of DGC retarded the development of amygdala kindling. Destruction of DGC after kindling was completed did not reverse the kindling effect. We conclude that DGC play a key role in the development, but not the permanence, of amygdala kindling. We propose a model whereby the greater the input to the hippocampal formation, the faster limbic kindling will proceed.

Full Text

Duke Authors

Cited Authors

  • Dasheiff, RM; McNamara, JO

Published Date

  • April 1982

Published In

Volume / Issue

  • 11 / 4

Start / End Page

  • 347 - 352

PubMed ID

  • 7103415

Pubmed Central ID

  • 7103415

International Standard Serial Number (ISSN)

  • 0364-5134

Digital Object Identifier (DOI)

  • 10.1002/ana.410110405

Language

  • eng

Conference Location

  • United States