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1 Department of Pharmacology, University of Virginia Health System, Charlottesville, Virginia, United States
* To whom correspondence should be addressed. E-mail: apb6w{at}virginia.edu.
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 (ChAT) was combined with TASK-3 labeling, using non-radioactive 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
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.
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