Quiroz, CésarGomes, CatarinaPak, Arlene C.Ribeiro, Joaquim A.Goldberg, Steven R.Hope, Bruce T.Ferré, Sergi2013-04-032013-04-032006The Journal of Neuroscience, October 18, 2006 • 26(42):10808 –108120270-6474http://dx.doi.org/10.1523/JNEUROSCI.1661-06.2006http://hdl.handle.net/10451/8188©2006 Society for NeurosciencePrevious studies have shown that cortical stimulation selectively activates extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation and immediate early gene expression in striatal GABAergic enkephalinergic neurons. In the present study, we demonstrate that blockade of adenosine A2A receptors with caffeine or a selective A2A receptor antagonist counteracts the striatal activation of cAMP– protein kinase A cascade (phosphorylation of the Ser845 residue of the glutamate receptor 1 subunit of the AMPA receptor) and mitogenactivated protein kinase (ERK1/2 phosphorylation) induced by the in vivo stimulation of corticostriatal afferents. The results indicate that A2A receptors strongly modulate the efficacy of glutamatergic synapses on striatal enkephalinergic neurons.engCaffeineAdenosine A2A receptorStriatumPhosphorylationERK1/2AMPA receptorBlockade of adenosine A2A receptors prevents protein phosphorylation in the striatum induced by cortical stimulationjournal article