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J Neurophysiol (December 1, 2002). 10.1152/jn.00361.2002
Submitted on 13 May 2002
Accepted on 1 August 2002
1Mental Retardation Research Center, University of California, Geffen School of Medicine, Los Angeles, California 90095; and 2Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, New York 10021
Flores-Hernández, Jorge,
Carlos Cepeda,
Elizabeth Hernández-Echeagaray,
Christopher R. Calvert,
Eve
S. Jokel,
Allen A. Fienberg,
Paul Greengard, and
Michael S. Levine.
Dopamine Enhancement of NMDA Currents in Dissociated Medium-Sized
Striatal Neurons: Role of D1 Receptors and DARPP-32. J. Neurophysiol. 88: 3010-3020, 2002. Dopamine
(DA), via activation of D1 receptors, enhances
N-methyl-D-aspartate (NMDA)-evoked responses in
striatal neurons. The present investigation examined further the
properties of this enhancement and the potential mechanisms by which
this enhancement might be effected. Dissociated medium-sized striatal
neurons were obtained from intact rats and mice or mutant mice lacking
the DA and cyclic adenosine 3',5' monophosphate (cAMP)-regulated
phosphoprotein of MR 32,000 (DARPP-32). NMDA (10-1,000 µM) induced inward currents in all
neurons. In acutely dissociated neurons from intact rats or mice,
activation of D1 receptors with the selective agonist, SKF 81297, produced a dose-dependent enhancement of NMDA currents. This
enhancement was reduced by the selective D1 receptor antagonist SKF
83566. Quinpirole, a D2 receptor agonist alone, produced small reductions of NMDA currents. However, it consistently and significantly reduced the enhancement of NMDA currents by D1 agonists. In dissociated striatal neurons, in conditions that minimized the contributions of
voltage-gated Ca2+ conductances, the D1-induced
potentiation was not altered by blockade of L-type voltage-gated
Ca2+ conductances in contrast to results in
slices. The DARPP-32 signaling pathway has an important role in D1
modulation of NMDA currents. In mice lacking DARPP-32, the enhancement
was significantly reduced. Furthermore, okadaic acid, a protein
phosphatase 1 (PP-1) inhibitor, increased D1-induced potentiation,
suggesting that constitutively active PP-1 attenuates D1-induced
potentiation. Finally, activation of D1 receptors produced differential
effects on NMDA and gamma aminobutyric acid (GABA)-induced currents in
the same cells, enhancing NMDA currents and inhibiting GABA currents.
Thus simultaneous activation of D1, NMDA, and GABA receptors could
predispose medium-sized spiny neurons toward excitation. Taken
together, the present findings indicate that the unique potentiation of
NMDA receptor function by activation of the D1 receptor signaling
cascade can be controlled by multiple mechanisms and has major
influences on neuronal function.
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