| First Author | Groblewski PA | Year | 2011 |
| Journal | Behav Brain Res | Volume | 217 |
| Issue | 2 | Pages | 399-407 |
| PubMed ID | 21074569 | Mgi Jnum | J:167235 |
| Mgi Id | MGI:4867591 | Doi | 10.1016/j.bbr.2010.11.018 |
| Citation | Groblewski PA, et al. (2011) Inhibition of extracellular signal-regulated kinase (ERK) activity with SL327 does not prevent acquisition, expression, and extinction of ethanol-seeking behavior in mice. Behav Brain Res 217(2):399-407 |
| abstractText | Although extracellular signal-regulated kinase (ERK) activity is essential for the acquisition of a variety of associative learning tasks, its involvement in the acquisition and extinction of ethanol (EtOH)-induced conditioned place preference (CPP) remains unknown. Therefore, in these experiments we examined the effects of the ERK-kinase (MEK)-inhibitor SL327 on acquisition and expression of EtOH-CPP as well as the dose- and time-dependent effects of SL327 on CPP extinction. The parametric findings of Experiment 1 showed that three 30-min (but not 15- or 5-min) non-reinforced trials were required to completely extinguish EtOH-CPP in male, DBA/2J mice. In Experiments 2 and 3, SL327 (30 and 50mg/kg), administered 30 or 90min prior to extinction trials, was unable to impair EtOH-CPP extinction. Experiment 4 showed that SL327 (50mg/kg) had no effect on acquisition of EtOH-CPP or the development of EtOH-induced sensitization during conditioning. When administered prior to testing in Experiments 5 and 6, SL327 did not alter expression of EtOH-CPP but did reduce test activity. Importantly, SL327 significantly reduced pERK protein levels when assessed in the dorsal striatum and motor cortex (Experiment 7). Together, these data suggest that EtOH-related learning and EtOH reward in mice, as assessed with CPP, are not impaired by the systemically administered MEK-inhibitor SL327. |
