Title

Expression of functional Kir6.1 channels regulates glutamate release at CA3 synapses in generation of epileptic form of seizures

Authors

Authors

M. M. Soundarapandian; D. Wu; X. F. Zhong; R. S. Petralia; L. S. Peng; W. H. Tu;Y. M. Lu

Comments

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Abbreviated Journal Title

J. Neurochem.

Keywords

excitotoxicity; K-ATP channels; seizure; K-ATP CHANNELS; SENSITIVE POTASSIUM CHANNELS; FOREBRAIN ISCHEMIA; METABOLIC SENSORS; CELL-DEATH; KAINATE; EXOCYTOSIS; NEURONS; CAMP; EXCITABILITY; Biochemistry & Molecular Biology; Neurosciences

Abstract

The Kir6.1 channels are a subtype of ATP-sensitive inwardly rectifying potassium (K-ATP) channels that play an essential role in coupling the cell's metabolic events to electrical activity. In this study, we show that functional Kir6.1 channels are located at excitatory pre-synaptic terminals as a complex with type-1 Sulfonylurea receptors (SUR1) in the hippocampus. The mutant mice with deficiencies in expressing the Kir6.1 or the SUR1 gene are more vulnerable to generation of epileptic form of seizures, compared to wild-type controls. Whole-cell patch clamp recordings demonstrate that genetic deletion of the Kir6.1/SUR1 channels enhances glutamate release at CA3 synapses. Hence, expression of functional Kir6.1/SUR1 channels inhibits seizure responses and possibly acts via limiting excitatory glutamate release.

Journal Title

Journal of Neurochemistry

Volume

103

Issue/Number

5

Publication Date

1-1-2007

Document Type

Article

Language

English

First Page

1982

Last Page

1988

WOS Identifier

WOS:000250985200026

ISSN

0022-3042

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