FGF acts as a co-transmitter through adenosine A(2A) receptor to regulate synaptic plasticity
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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.
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Nat. Neurosci.
Nat. Neurosci. 11(12): 1402-9
26th Oct 2008
Marc Flajolet, Zhongfeng Wang, Marie Futter, Weixing Shen, Nina Nuangchamnong, Jacob Bendor, Iwona Wallach, Angus C Nairn, D James Surmeier, Paul Greengard
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- Created: 4th Jan 2013 at 11:25
- Last updated: 24th Oct 2013 at 16:22
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