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• W2023668469 abstract "This study examined whether activation of extracellular signal-regulated kinase (ERK) contributes to the increased open-arm time observed in the elevated plus maze (EPM) during opioid withdrawal. We applied SL327, a selective ERK kinase (MEK) inhibitor, to specific limbic areas and examined the effect on EPM behaviors of controls and during naloxone-precipitated morphine withdrawal. We next confirmed that ERK activation increased in limbic areas of mice undergoing naloxone-precipitated morphine withdrawal. Direct injection of SL327 into the amygdala blocked the withdrawal-induced increase in open-arm time; however, injecting SL327 into the septum had no effect. Consistent with these results, both 0.2 and 2 mg/kg naloxone increased ERK activation in the central amygdala of morphine-dependent mice. In drug-naive mice, 2 mg/kg naloxone, but not 0.2 mg/kg, increased ERK activation in the central amygdala. During withdrawal, increased ERK activation was also observed in the lateral septum. In the locus coeruleus, a significant increase was observed only in morphine-dependent mice receiving 2 mg/kg, but not 0.2 mg/kg naloxone. In conclusion, ERK activation in limbic areas is likely involved in both the aversive properties of naloxone and in the affective/emotional symptoms of opioid withdrawal, including mediating EPM behaviors." @default.
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• W2023668469 date "2009-10-01" @default.
• W2023668469 modified "2023-09-23" @default.
• W2023668469 title "Extracellular signal-regulated kinase activation in the amygdala mediates elevated plus maze behavior during opioid withdrawal" @default.
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• W2023668469 doi "https://doi.org/10.1097/fbp.0b013e32832ec57e" @default.
• W2023668469 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4494789" @default.
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