These studies suggest that both forms of pre-exposure reduced ethanol's aversive effect, but had no impact on ethanol's rewarding effect. In general, the detrimental effects of pre-exposure on CPA are explained best in terms of a reduction in ethanol's efficacy as an aversive unconditioned stimulus (i.e. tolerance), although explanations based on other types of associative interference are also possible. The failure to affect CPP with pre-exposure treatments that reduced or eliminated CPA suggests that these behaviors are mediated by independent, motivationally opposite effects of ethanol. Moreover, these results indicate dissociation between sensitization to ethanol's locomotor activating effect and changes in its rewarding effect. To the extent that motivational processes measured by CPP and CPA normally contribute to ethanol drinking, the present findings suggest that increases in ethanol intake seen after chronic ethanol exposure are more likely caused by tolerance to ethanol's aversive effect rather than sensitization to its rewarding or reinforcing effect.

We have identified a number of previously unrecognized barriers to and enablers for prehospital pediatric analgesia. The majority of these factors lead to an overall preference of paramedics to defer administration of analgesic agents. A number of educational and EMS system changes could be made to address these barriers and increase the frequency of appropriate pediatric prehospital analgesia.

These findings suggest that the conditioned reinforcing effects of ethanol in DBA/2J mice as assessed by place conditioning are mediated by non-dopaminergic mechanisms.

No abstract