NDLI: Activation of ATP-sensitive $K^{+}$ $(K_{ATP})$ channels by $H_{2}O_{2}$ underlies glutamate-dependent inhibition of striatal dopamine release

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Activation of ATP-sensitive $K^{+}$ $(K_{ATP})$ channels by $H_{2}O_{2}$ underlies glutamate-dependent inhibition of striatal dopamine release

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Activation of ATP-sensitive $K^{+}$ $(K_{ATP})$ channels by $H_{2}O_{2}$ underlies glutamate-dependent inhibition of striatal dopamine release

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Rice, Margaret E. Avshalumov, Marat V.
Description	Author Affiliation: Avshalumov MV ( Department of Physiology, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.);
Abstract	In many cells, ATP-sensitive K+ channels (KATP channels) couple metabolic state to excitability. In pancreatic beta cells, for example, this coupling regulates insulin release. Although KATP channels are abundantly expressed in the brain, their physiological role and the factors that regulate them are poorly understood. One potential regulator is H2O2. We reported previously that dopamine (DA) release in the striatum is modulated by endogenous H2O2, generated downstream from glutamatergic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-receptor activation. Here we investigated whether H2O2-sensitive KATP channels contribute to DA-release modulation by glutamate and gamma-aminobutyric acid (GABA). This question is important because DA-glutamate interactions underlie brain functions, including motor control and cognition. Synaptic DA release was evoked by using local electrical stimulation in slices of guinea pig striatum and monitored in real time with carbon-fiber microelectrodes and fast-scan cyclic voltammetry. The KATP-channel antagonist glibenclamide abolished the H2O2-dependent increase in DA release usually seen with AMPA-receptor blockade by GYKI-52466 [1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine hydrochloride] and the decrease in DA release seen with GABA-type-A-receptor blockade by picrotoxin. In contrast, 5-hydroxydecanoate, a mitochondrial KATP-channel blocker, was ineffective, as were sulpiride, a D2-receptor antagonist, and tertiapin, a G protein-coupled K+-channel inhibitor. Diazoxide, a sulfonylurea receptor 1 (SUR1)selective KATP-channel opener, prevented DA modulation by H2O2, glutamate, and GABA, whereas cromakalim, a SUR2-selective opener, did not. Thus, endogenous H2O2 activates SUR1-containing KATP channels in the plasma membrane to inhibit DA release. These data not only demonstrate that KATP channels can modulate CNS transmitter release in response to fast-synaptic transmission but also introduce H2O2 as a KATP-channel regulator.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	20
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adenosine Triphosphate Metabolism Corpus Striatum Drug Effects Dopamine Pharmacology Hydrogen Peroxide Potassium Channels Animals Guinea Pigs In Vitro Techniques Mitochondria Receptors, Dopamine D2 Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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