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Cerebral Cortex Advance Access published online on August 9, 2007
Cerebral Cortex, doi:10.1093/cercor/bhm133
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© The Author 2007. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Dopamine Modulation of Prefrontal Cortex Interneurons Occurs Independently of DARPP-32

Heather Trantham-Davidson*, Sven Kröner* and Jeremy K. Seamans

Medical University of South Carolina, Department of Neuroscience, BSB 403, 173 Ashley Avenue, Charleston, SC 29425

Address correspondence to Jeremy K. Seamans, PhD, Dept of Psychiatry, University of British Columbia, Brain Research Centre, 2211 Wesbrook Mall, Vancouver, BC, V6T 2B5, Canada. Email: seamans{at}interchange.ubc.ca.

Dopamine (DA) exerts a strong influence on inhibition in prefrontal cortex. The main cortical interneuron subtype targeted by DA are fast-spiking {gamma}-aminobutyric acidergic (GABAergic) cells that express the calcium-binding protein parvalbumin. D1 stimulation depolarizes these interneurons and increases excitability evoked by current injection. The present study examined whether this direct DA-dependent modulation of fast-spiking interneurons involves DARPP-32. Whole-cell patch-clamp recordings were made from fast-spiking interneurons in brain slices from DARPP-32 knockout (KO) mice, wild-type mice, and rats. Low concentrations of DA (100 nM) increased interneuron excitability via D1 receptors, protein kinase A, and cyclic adenosine 3',5'-monophosphate in slices from both normal and DARPP-32 KO mice. Immunohistochemical staining of slices from normal animals revealed a lack of colocalization of DARPP-32 with calcium-binding proteins selective for fast-spiking interneurons, indicating that these interneurons do not express DARPP-32. Therefore, although DARPP-32 impacts cortical inhibition through a previously demonstrated D2-dependent regulation of GABAergic currents in pyramidal cells, it is not involved in the direct D1-mediated regulation of fast-spiking interneurons.

Key Words: D1 • GABA • inhibition • PFC • schizophrenia

* The first 2 authors contributed equally to the present study


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