FGF acts as a co-transmitter through adenosine A(2A) receptor to regulate synaptic plasticity. Export

@article{citeulike:3468210, abstract = {Abnormalities of striatal function have been implicated in several major neurological and psychiatric disorders, including Parkinson's disease, schizophrenia and depression. Adenosine, via activation of A(2A) receptors, antagonizes dopamine signaling at D2 receptors and A(2A) receptor antagonists have been tested as therapeutic agents for Parkinson's disease. We found a direct physical interaction between the G protein-coupled A(2A) receptor (A(2A)R) and the receptor tyrosine kinase fibroblast growth factor receptor (FGFR). Concomitant activation of these two classes of receptors, but not individual activation of either one alone, caused a robust activation of the MAPK/ERK pathway, differentiation and neurite extension of PC12 cells, spine morphogenesis in primary neuronal cultures, and cortico-striatal plasticity that was induced by a previously unknown A(2A)R/FGFR-dependent mechanism. The discovery of a direct physical interaction between the A(2A) and FGF receptors and the robust physiological consequences of this association shed light on the mechanism underlying FGF functions as a co-transmitter and open new avenues for therapeutic interventions.}, author = {Flajolet, Marc and Wang, Zhongfeng and Futter, Marie and Shen, Weixing and Nuangchamnong, Nina and Bendor, Jacob and Wallach, Iwona and Nairn, Angus C C. and Surmeier, D James J. and Greengard, Paul}, citeulike-article-id = {3468210}, citeulike-linkout-0 = {http://dx.doi.org/10.1038/nn.2216}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/18953346}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=18953346}, day = {26}, doi = {10.1038/nn.2216}, issn = {1546-1726}, journal = {Nature neuroscience}, keywords = {a2a, fgf, plasticity}, month = {October}, posted-at = {2008-10-31 11:00:53}, priority = {4}, title = {FGF acts as a co-transmitter through adenosine A(2A) receptor to regulate synaptic plasticity.}, url = {http://dx.doi.org/10.1038/nn.2216}, year = {2008} }

TY - JOUR ID - citeulike:3468210 L3 - citeulike-article-id:3468210 N2 - Abnormalities of striatal function have been implicated in several major neurological and psychiatric disorders, including Parkinson's disease, schizophrenia and depression. Adenosine, via activation of A(2A) receptors, antagonizes dopamine signaling at D2 receptors and A(2A) receptor antagonists have been tested as therapeutic agents for Parkinson's disease. We found a direct physical interaction between the G protein-coupled A(2A) receptor (A(2A)R) and the receptor tyrosine kinase fibroblast growth factor receptor (FGFR). Concomitant activation of these two classes of receptors, but not individual activation of either one alone, caused a robust activation of the MAPK/ERK pathway, differentiation and neurite extension of PC12 cells, spine morphogenesis in primary neuronal cultures, and cortico-striatal plasticity that was induced by a previously unknown A(2A)R/FGFR-dependent mechanism. The discovery of a direct physical interaction between the A(2A) and FGF receptors and the robust physiological consequences of this association shed light on the mechanism underlying FGF functions as a co-transmitter and open new avenues for therapeutic interventions. JF - Nature neuroscience SN - 1546-1726 TI - FGF acts as a co-transmitter through adenosine A(2A) receptor to regulate synaptic plasticity. KW - a2a KW - fgf KW - plasticity AU - Flajolet, Marc AU - Wang, Zhongfeng AU - Futter, Marie AU - Shen, Weixing AU - Nuangchamnong, Nina AU - Bendor, Jacob AU - Wallach, Iwona AU - Nairn, Angus C AU - Surmeier, D James AU - Greengard, Paul PY - 2008/10/26/ UR - http://dx.doi.org/10.1038/nn.2216 ER -