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J. Biol. Chem., Vol. 283, Issue 23, 15799-15806, June 6, 2008

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Dopamine D1 Receptor-induced Signaling through TrkB Receptors in Striatal Neurons^*

Yuriko Iwakura¹, Hiroyuki Nawa, Ichiro Sora^¶, and Moses V. Chao²

From the Molecular Neurobiology Program, Kimmel Center at Skirball Institute of Biomolecular Medicine, Departments of Cell Biology, Physiology and Neuroscience, and Psychiatry, New York University School of Medicine, New York, New York 10016, the Division of Molecular Neurobiology, Brain Research Institute, Niigata University, 1-757 Asahimachi, Niigata, 951-8585, Japan, and the ^¶Department of Biological Psychiatry, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Sendai, 980-8574, Japan

In addition to its role as a neurotransmitter, dopamine can stimulate neurite outgrowth and morphological effects upon primary neurons. To investigate the signal transduction mechanisms used by dopamine in developing striatal neurons, we focused upon the effects of activating the dopamine D1 receptor. Using the D1 receptor agonist SKF38393, we found that Trk neurotrophin receptors were activated in embryonic day 18 striatal neurons. K-252a, a Trk tyrosine kinase inhibitor, and a dopamine D1 receptor antagonist could block the effects of SKF38393. The increase in TrkB phosphorylation was not the result of increased neurotrophin production. Induction of TrkB activity by SKF38393 was accompanied by the phosphorylation of several Trk signaling proteins, including phospholipase C, Akt, and MAPK. Biotinylation experiments followed by immunostaining by phospho-TrkB-specific antibodies indicated that the mechanism involved increased TrkB surface expression by dopamine D1 receptor activation. This increase in cell surface TrkB expression was dependent upon an increase in intracellular Ca²⁺. These results indicate that stimulation of dopamine D1 receptors can be coupled to the neurotrophin receptor signaling to mediate the effects of dopamine upon striatal neurons.

Received for publication, February 26, 2008 , and in revised form, March 27, 2008.

^* This work was supported, in whole or in part, by National Institutes of Health Grants NS21072 and HD23315 (to M. V. C.). This work was also supported by grants from the Core Research for Evolutional Science and Technology from Japan Science and Technology Agency (to H. N. and I. S.) and a grant for the promotion of a Niigata University Research Project (to H. N.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Supported by postdoctoral fellowship from the Uehara Memorial Foundation. Present address: Division of Molecular Neurobiology, Brain Research Institute, Niigata University, 1-757 Asahimachi, Niigata, 951-8585, Japan.

² To whom correspondence should be addressed: Molecular Neurobiology, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, 540 1st Ave., New York, NY 10016. E-mail: chao{at}saturn.med.nyu.edu.

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