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Schizophrenia Bulletin Advance Access originally published online on September 28, 2007
Schizophrenia Bulletin 2007 33(6):1263-1269; doi:10.1093/schbul/sbm106
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© The Author 2007. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Ether-a-go-go–Related Gene Potassium Channels: What's All the Buzz About?

Paul D. Shepard1,2, Carmen C. Canavier3 and Edwin S. Levitan4
2 Maryland Psychiatric Research Center and Department of Psychiatry, University of Maryland School of Medicine, PO Box 21247, Baltimore, MD 21228
3 Neuroscience Center for Excellence and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, LA 70112
4 Department of Pharmacology, University of Pittsburgh, Pittsburgh, PA 15261

1 To whom correspondence should be addressed; tel: 410-402-7753, fax: 410-402-6066, e-mail: pshepard{at}mprc.umaryland.edu.

Antipsychotic drugs are thought to exert their therapeutic action by antagonizing dopamine receptors but are also known to produce side effects in the heart by inhibiting cardiac ether-a-go-go–related gene (ERG) K+ channels. Recently, it has been discovered that the same channels are present in the brain, including midbrain dopamine neurons. ERG channels are most active after the cessation of intense electrical activity, and blockade of these channels prolongs plateau potentials in bursting dopamine neurons. This change in excitability would be expected to alter dopamine release. Therefore, the therapeutic action of antipsychotic drugs may depend on inhibition of both postsynaptic dopamine receptors and presynaptic ERG K+ channels.

Keywords: schizophrenia / bursting / dopamine / antipsychotic drugs / review


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Home page
 J. Physiol.Home page
P. D. Shepard and M. C. Trudeau
Emerging roles for ether-a-go-go-related gene potassium channels in the brain
J. Physiol., October 15, 2008; 586(20): 4785 - 4786.
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