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The Journal of Neuroscience, April 6, 2005, 25(14):3712-3723; doi:10.1523/JNEUROSCI.5389-03.2005

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Cellular/Molecular
Rapid Upregulation of 7 Nicotinic Acetylcholine Receptors by Tyrosine Dephosphorylation

Chang-Hoon Cho,¹ Weifeng Song,¹ Katherine Leitzell,² Esther Teo,³ Annal D. Meleth,¹ Michael W. Quick,^2,3 and Robin A. J. Lester¹

¹Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, and ²Neuroscience Graduate Program and ³Department of Biological Sciences, University of Southern California, Los Angeles, California 90089

7 nicotinic acetylcholine receptors (nAChRs) modulate network activity in the CNS. Thus, functional regulation of 7 nAChRs could influence the flow of information through various brain nuclei. It is hypothesized here that these receptors are amenable to modulation by tyrosine phosphorylation. In both Xenopus oocytes and rat hippocampal interneurons, brief exposure to a broad-spectrum protein tyrosine kinase inhibitor, genistein, specifically and reversibly potentiated 7 nAChR-mediated responses, whereas a protein tyrosine phosphatase inhibitor, pervanadate, caused depression. Potentiation was associated with an increased expression of surface 7 subunits and was not accompanied by detectable changes in receptor open probability, implying that the increased function results from an increased number of 7 nAChRs. Soluble N-ethylmaleimide-sensitive factor attachment protein receptor-mediated exocytosis was shown to be a plausible mechanism for the rapid delivery of additional 7 nAChRs to the plasma membrane. Direct phosphorylation/dephosphorylation of 7 subunits was unlikely because mutation of all three cytoplasmic tyrosine residues did not prevent the genistein-mediated facilitation. Overall, these data are consistent with the hypothesis that the number of functional cell surface 7 nAChRs is controlled indirectly via processes involving tyrosine phosphorylation.

Key words: addiction; hippocampus; protein kinase; protein phosphatase; receptor turnover; exocytosis

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Received Dec 5, 2003; revised March 2, 2005; accepted March 2, 2005.

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