Role of K-ATP channels in protection against neuronal excitatory insults

    Authors

    M. M. Soundarapandian; X. F. Zhong; L. S. Peng; D. Wu;Y. M. Lu

    Comments

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    Abbreviated Journal Title

    J. Neurochem.

    Keywords

    epilepsy; excitotoxicity; glutamate; ischemia; K-ATP; synaptic; degeneration; SENSITIVE POTASSIUM CHANNELS; PERSISTENT HYPERINSULINEMIC HYPOGLYCEMIA; MITOCHONDRIAL PERMEABILITY TRANSITION; METABOTROPIC GLUTAMATE RECEPTORS; STRIATAL DOPAMINE RELEASE; HIPPOCAMPAL CA1 NEURONS; TRAUMATIC; BRAIN-INJURY; CAMP SENSOR EPAC; FAMILIAL HYPERINSULINISM; SULFONYLUREA; RECEPTOR-1; Biochemistry & Molecular Biology; Neurosciences

    Abstract

    ATP-sensitive K+ (K-ATP) channels that are gated by intracellular ATP/ADP concentrations are a unique subtype of potassium channels and play an essential role in coupling intracellular metabolic events to electrical activity. Opening of K-ATP channels during energy deficits in the CNS induces efflux of potassium ions and in turn hyperpolarizes neurons. Thus, activation of K-ATP channels is thought to be able to counteract excitatory insults and protect against neuronal death. In this review, we bring together recent studies about what kinds of molecules are needed to build and regulate arrays of K-ATP channel functions in the CNS neurons. We propose a model to explain how K-ATP channel activation regulates glutamate release from the pre-synaptic terminals and how this regulation protects against ischemic neuronal injury and epilepsy.

    Journal Title

    Journal of Neurochemistry

    Volume

    103

    Issue/Number

    5

    Publication Date

    1-1-2007

    Document Type

    Review

    Language

    English

    First Page

    1721

    Last Page

    1729

    WOS Identifier

    WOS:000250985200003

    ISSN

    0022-3042

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