TI - Roles of the AMPA receptor subunit GluA1 but not GluA2 in synaptic potentiation and activation of ERK in the anterior cingulate cortex . AB - Cortical areas including the anterior cingulate cortex ( ACC ) are important for pain and pleasure . Recent studies using genetic and physiological approaches have demonstrated that the investigation of basic mechanism for long-term potentiation ( LTP ) in the ACC may reveal key cellular and molecular mechanisms for chronic pain in the cortex . Glutamate N-methyl D-aspartate ( NMDA ) receptors in the ACC are critical for the induction of LTP , including both NR2A and NR2B subunits . However , cellular and molecular mechanisms for the expression of ACC LTP have been less investigated . Here , we report that the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid ( AMPA ) receptor subunit , GluA1 contributes to LTP in the ACC using genetic manipulated mice lacking GluA1 or GluA2 gene . Furthermore , GluA1 knockout mice showed decreased extracellular signal-regulated kinase ( ERK ) PHOSphorylation in the ACC in inflammatory pain models in vivo . Our results demonstrate that AMPA receptor subunit GluA1 is a key mechanism for the expression of ACC LTP and inflammation-induced long-term plastic changes in the ACC .