Intradentate colchicine retards the development of amygdala kindling.
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.
Duke Scholars
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- Rats
- Neurology & Neurosurgery
- Kindling, Neurologic
- Hippocampus
- Epilepsy
- Disease Models, Animal
- Colchicine
- Animals
- Amygdala
- 3209 Neurosciences
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Rats
- Neurology & Neurosurgery
- Kindling, Neurologic
- Hippocampus
- Epilepsy
- Disease Models, Animal
- Colchicine
- Animals
- Amygdala
- 3209 Neurosciences