Comparison of the MK-801-induced appetitive extinction deficit with pressing for reward and associated pERK1/2 staining in prefrontal cortex and nucleus accumbens

摘要: Administration of the noncompetitive N-methyl-d-aspartate (NMDA)-receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) has been shown to produce extinction deficits on appetitive operant tasks. The present study sought further explore this by comparing pressing for primary reward and examining associated neural correlates determine if MK-801 profile resembled behavioral with reward. Immunohistochemical labeling phosphorylated extracellular signal-regulated kinase-1 -2(pERK1/2) in prelimbic (PrL) infralimbic (IL) cortices nucleus accumbens shell (AcbSh) core (AcbC) was examined after rewarded or lever conditions. A dose-response curve revealed a within-day deficit following administration 0.05 mg/kg MK-801. All doses were reduced IL pERK1/2 staining but only dose elevated AcbSh labeling. Extinction under influence compared that seen during pressing-whether saline. Rewarded saline PrL no similar patterns MK-801/extinction group. There more group than any other condition. These data suggest MK-801-induced may be due combination an underactive cortical inhibition system overactive system.