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

    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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