Alterations of the Cerebellar Inhibitory Interneurons and Inhibitory Synapse Following KA-induced Seizures.
- Author:
So Young LEE
1
;
Jong Hwan LEE
;
You Jin WON
;
Seung Yong YUN
;
Seung Jun HWANG
;
Jong Uk KIM
;
Donghou KIM
;
Hea Nam HONG
Author Information
1. Department of Anatomy and Cell Biology, University of Ulsan College of Medicine, Korea. hnhong@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
Kainic acid;
Cerebellar inhibitory interneuron;
Cerebellar inhibitory synapse;
GAP-43;
GABA
- MeSH:
Blotting, Western;
Depression;
gamma-Aminobutyric Acid;
GAP-43 Protein;
Humans;
Immunohistochemistry;
Interneurons*;
Kainic Acid;
Microscopy, Confocal;
Presynaptic Terminals;
Purkinje Cells;
Seizures*;
Synapses*;
Synaptic Transmission
- From:Korean Journal of Anatomy
2005;38(2):153-166
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Most epileptic patients have commonly suffered from recurrent seizures for many years. These seizures are usually associated with inhibitory synaptic reorganization of the hippocampal region, but it is not known whether cerebellar inhibitory synaptic changes can be induced by seizure activity. We sought to determine the pattern of cerebellar alterations in the cerebellar inhibitory interneurons (basket and stellate cells) and then tested if the alterations are associated with their synaptic transmission at the cerebellar GABAergic synapses between inhibitory interneurons and Purkinje cells after systemic kainic acid administration by immunohistochemistry, western blot analysis, dot blot analysis and confocal microscopy. A dramatic increase of the intensity of GAP-43 immunostaining was obvious in the pinceau structures following KA-induced seizures and the intense GAP-43 immunoreaction involved in high expression of PKC-sigma. The activation of the presynaptic terminal at the cerebellar inhibitory synapse is accompanied with strong GABA immunoreactivity in pinceau region (especially 48 h) after KA-seizures. These results suggest a possibility that KA-seizures increase the release of GABA at the cerebellar inhibitory presynaptic terminal and it would be contribute to the depression of Purkinje cell activity, disinhibition, during the epileptogenesis.
