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Papers In Press, published online ahead of print December 16, 2003
Department of Microbiology, University of Virginia, Charlottesville, VA 22908
Corresponding Author: sap{at}virginia.edu
Src family kinases (SFKs) are abundant in chromaffin cells that reside in the adrenal medulla and respond to cholinergic stimulation by secreting catecholamines. Our previous work indicated that SFKs regulate acetylcholine - or nicotine-induced secretion, but the site of modulatory action was unclear. Using whole cell recordings, we found that inhibition of SFK tyrosine kinase activity by PP2 treatment or expression of a kinase-defective c-Src reduced the peak amplitude of nicotine-induced currents in chromaffin cells or in human embryonic kidney cells (HEK293) ectopically expressing functional neuronal
J. Biol. Chem, 10.1074/jbc.M309652200
Submitted on September 2, 2003
Revised on November 24, 2003
Accepted on December 16, 2003
Regulation of the neuronal nicotinic acetylcholine receptor by Src family tyrosine kinases
3
45 acetylcholine receptors (AChR). Conversely, the phosphotyrosine phosphatase (PTPase) inhibitor, sodium vanadate, or expression of mutationally activated c-Src resulted in enhanced current amplitudes. These results suggest that SFKs and putative PTPases regulate the activity of AChRs by opposing actions. This proposed model was further supported by the findings that SFKs physically associate with the receptor and that the AChR is tyrosine phosphorylated.
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