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J Neurophysiol 97: 1546-1552, 2007. First published December 13, 2006; doi:10.1152/jn.01090.2006
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Striatal Cholinergic Interneurons Express a Receptor-Insensitive Homomeric TASK-3–Like Background K+ Current

Allison P. Berg1 and Douglas A. Bayliss1,2

1Departments of Pharmacology and 2Anesthesiology, University of Virginia, Charlottesville, Virginia

Submitted 11 October 2006; accepted in final form 7 December 2006

Large aspiny cholinergic interneurons provide the sole source of striatal acetylcholine, a neurotransmitter essential for normal basal ganglia function. Cholinergic interneurons engage in multiple firing patterns that depend on interactions among various voltage-dependent ion channels active at different membrane potentials. Leak conductances, particularly leak K+ channels, are of primary importance in establishing the prevailing membrane potential. We have combined molecular neuroanatomy with whole cell electrophysiology to demonstrate that TASK-3 (K2P9.1, Kcnk9) subunits contribute to leak K+ currents in striatal cholinergic interneurons. Immunostaining for choline acetyltransferase was combined with TASK-3 labeling, using nonradioactive cRNA probes or antisera selective for TASK-3, to demonstrate that striatal cholinergic neurons universally express TASK-3. Consistent with this, we isolated a pH-, anesthetic-, and Zn2+-sensitive current with properties expected of TASK-3 homodimeric channels. Surprisingly, activation of G{alpha}q-linked receptors (metabotropic glutamate mGluR1/5 or histamine H1) did not appear to modulate native interneuron TASK-3–like currents. Together, our data indicate that homomeric TASK-3–like background K+ currents contribute to establishing membrane potential in striatal cholinergic interneurons and they suggest that receptor modulation of TASK channels is dependent on cell context.


Address for reprint requests and other correspondence: A. P. Berg, Department of Pharmacology, Box 800735, 5015 Jordan Hall, University of Virginia, Charlottesville, VA 22908 (E-mail: apb6w{at}virginia.edu)




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