Significant differences were found in one or both groups for the prevalence of frequent cocaine injection, requiring help injecting, binge drug use, residence in the HIV outbreak epicentre, sex-trade participation and syringe sharing (all p < 0.05) after incarceration.
In models adjusted for age, gender and Aboriginal ethnicity, no significant differences were found in the prevalence of frequent cocaine injection (p = 0.737); needing help injecting (p = 0.201); binge drug use (p = 0.273); living in the DTES (p = 0.105) or participation in the sex trade (p = 0.623) before and after a period of incarceration compared to a matched control group.
An association between injecting site infections in England has been reported with crack cocaine injection and elsewhere with cocaine injection (2, 3, 7 ).
Increases in MAP (∼25 mm Hg) following cocaine injection were dose-dependently attenuated by mAb 15A10.
Sensitization also developed to the antinociceptive effect of cocaine 24 h but not 1 wk after the last cocaine injection.
pretreatments of either mAb 15A10 (10, 32, 100 and 300 mg/kg) or vehicle prior to cocaine injection (100 mg/kg, i.p).
After 30 days of abstinence, the reactivity of the reward system was assessed with functional magnetic resonance imaging (fMRI) following an intravenous cocaine injection challenge.
Naı̈ve rats were injected with either saline or cocaine (30 mg/kg) once daily for 3 days and tested on the hot plate apparatus either 24 h or 1 wk after the last cocaine injection.
On day 10, cocaine challenge of rats treated repeatedly with the psychostimulant (days 1 5) significantly enhanced locomotor hyperactivity compared to the effect of acute cocaine injection in saline-treated (days 1 5) animals.
Expression of the dnTrkB transgene not only prevented the acute cocaine-induced increase in p-TrkB, but it also prevented behavioral sensitization and CPP following a single cocaine injection.
Specifically, LFP activity was highest during the first 30 min following the cocaine injection and was most robust in Delta and Theta frequency bands; indicating the role of low frequency VTA activity in the initiation of acute stimulant-induced locomotor behavior.
