What accounts for differences in HIV stigma across different high prevalence settings? This study was designed to examine HIV stigma and discrimination in five high prevalence settings. Qualitative data were collected as part of the US National Institute of Mental Health (NIMH) Project Accept, a multi-site community randomized trial of community-based HIV voluntary counseling and testing. In-depth interviews were conducted with 655 participants in five sites, four in Sub-Saharan Africa and one in Southeast Asia. Interviews were conducted in the local languages by trained research staff. Data were audiotaped, transcribed, translated, coded and computerized for thematic data analysis. Participants described the stigmatizing attitudes and behaviors perpetuated against people living with HIV/AIDS (PLWHA). The factors that contribute to HIV stigma and discrimination include fear of

Electrophysiological studies have demonstrated that dopaminergic neurons burst fire during certain aspects of rewardrelated behavior; however, the correlation between dopamine release and cell firing is unclear. When complex stimulation patterns that mimic intracranial self-stimulation were employed, dopamine release was shown to exhibit facilitated as well as depressive components (Montague et al. 2004). Understanding the biological mechanisms underlying these variations in dopamine release is necessary to unravel the correlation between unit activity and neurotransmitter release. The dopamine autoreceptor provides negative feedback to dopamine release, inhibiting release on the time scale of a few seconds. Therefore, we investigated this D 2 receptor to see whether it is one of the biological mechanisms responsible for the history-dependent modulation of dopamine release.Striatal dopamine release in anesthetized rats was evoked with stimulus trains that were designed to promote the variability of dopamine release. Consistent with the well established D 2 -mediated autoinhibition, the short-term depressive component of dopamine release was blocked by raclopride, a D 2 antagonist, and enhanced by quinpirole, a D 2 -receptor agonist. Surprisingly, these same drugs exerted a similar effect on the short-term facilitated component: a decrease with raclopride and an increase with quinpirole. These data demonstrate that the commanding control exerted by dopamine autoreceptors over short-term neuroadaptation of dopamine release involves both inhibitory and paradoxically, facilitatory components.

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The ventral tegmental area (VTA), the locus of mesolimbic dopamine cell bodies, contains dopamine. Experiments in brain slices have demonstrated that VTA dopamine can be released by local electrical stimulation. Measurements with both push-pull cannula and microdialysis in intact animals have also obtained evidence for releasable dopamine. Here we demonstrate that dopamine release in the VTA can be evoked by remote stimulations of the medial forebrain bundle (MFB) in the anesthetized rat. In initial experiments, the MFB was electrically stimulated while a carbon-fiber electrode was lowered to the VTA, with recording by fast-scan cyclic voltammetry. While release was not observed with the carbon fiber 4 to 6 mm below dura, a voltammetric response was observed a t 6-8 mm below dura, but the voltammogram was poorly defined. At lower depths, in the VTA, dopamine release was evoked. Immunohistochemistry experiments with antibodies for tyrosine hydroxylase (TH) confirmed that dopamine processes were primarily found below 8 mm. Similarly, tissue content determined by liquid chromatography revealed serotonin but not dopamine dorsal to 8 mm with both dopamine and serotonin at lower depths. Evaluation of the VTA signal by pharmacological means showed that it increased with inhibitors of dopamine uptake, but release was not altered by D2 agents. Dopamine release in the VTA was frequency dependent and could be exhausted by stimulations longer than 5 s. Thus, VTA dopamine release can be evoked in vivo by remote stimulations and it resembles release in terminal regions, possessing a similar uptake mechanism and a finite releasable storage pool.

As part of a larger study to examine the feasibility and acceptability of a couples-based HIV-prevention intervention, we conducted formative in-depth interviews with 10 couples to explore topics such as challenges in practising safer sex, HIV-prevention strategies, gender power and violence, and issues of trust and infidelity. In this study, both men and women perceived infidelity as ubiquitous in their social context and were therefore unable to discuss HIV risk and prevention without suspicions of infidelity in their own relationship. This impacted couples’ ability openly and effectively to discuss strategies to prevent HIV and thus may have contributed to the limited uptake of HIV-prevention strategies, such as condom use and HIV testing. The contentious nature of safe-sex discussions placed both members of the couple at a higher risk for HIV acquisition within the partnership. This study sheds light on how existing relationship norms in South Africa influence HIV-prevention communication within couples and suggests that new ways of approaching conflictual issues such as mistrust and infidelity are vital in order for HIV-prevention programmes to succeed.