Examining the Crack Epidemic and Subsequent Drug Policy through Identifying Trends in Outpatient Substance Abuse Treatment for Crack Use/Abuse: 1995-2005

Disparities in the crack/cocaine discourse have changed drastically since its inception over 30 years ago. Since the late 1980s, research examining this particular abuse has become more complex as both nationally and globally crack use/abuse has been examined within various contexts. Crack use has often been framed as an African American problem in part resulting from the high volume of African Americans seeking treatment for illnesses associated with their crack-cocaine use, and more African Americans dying from crack-cocaine overdose. This logical fallacy persists despite evidence showing African Americans have lower substance use/abuse compared to Caucasians. Given the impact of the crack epidemic as well as its related drug policies on African American communities and their families, further examination of crack use/abuse is necessary. This study will discuss the crack epidemic historically and examine crack use among clients of a large sample of outpatient substance abuse treatment units over a decade period between 1995 and 2005.

Enhanced rewarding properties of morphine, but not cocaine, in beta(arrestin)-2 knock-out mice.

The reinforcing and psychomotor effects of morphine involve opiate stimulation of the dopaminergic system via activation of mu-opioid receptors (muOR). Both mu-opioid and dopamine receptors are members of the G-protein-coupled receptor (GPCR) family of proteins. GPCRs are known to undergo desensitization involving phosphorylation of the receptor and the subsequent binding of beta(arrestins), which prevents further receptor-G-protein coupling. Mice lacking beta(arrestin)-2 (beta(arr2)) display enhanced sensitivity to morphine in tests of pain perception attributable to impaired desensitization of muOR. However, whether abrogating muOR desensitization affects the reinforcing and psychomotor properties of morphine has remained unexplored. In the present study, we examined this question by assessing the effects of morphine and cocaine on locomotor activity, behavioral sensitization, conditioned place preference, and striatal dopamine release in beta(arr2) knock-out (beta(arr2)-KO) mice and their wild-type (WT) controls. Cocaine treatment resulted in very similar neurochemical and behavioral responses between the genotypes. However, in the beta(arr2)-KO mice, morphine induced more pronounced increases in striatal extracellular dopamine than in WT mice. Moreover, the rewarding properties of morphine in the conditioned place preference test were greater in the beta(arr2)-KO mice when compared with the WT mice. Thus, beta(arr2) appears to play a more important role in the dopaminergic effects mediated by morphine than those induced by cocaine.