Cocaine functioned as a positive reinforcer in a dose-related manner in all monkeys.
Initially, the use of crack cocaine functioned as an informal harm reduction strategy.
This indicates that the inhibitory deficit increases as a function of the history of cocaine use [2], [11].
The magnitude of the shift to the right in the cocaine dose response function was directly related to PB dose.
or the descending limb (0.75 mg/kg, i.v). of the cocaine dose effect function.
limbs of the cocaine dose effect function, with the latter effect blocked by the 5-HT1B receptor antagonist SB 224289 (5.0 mg/kg, i.p.; Figure 4).
Specifically, during ongoing maintenance of self-administration, viral-mediated 5-HT1B-receptor gene transfer shifts the cocaine dose effect function upward and to the left on a FR5 schedule, and increases breakpoints and cocaine intake on a PR schedule.
In contrast, in rats, 5-HT1B receptor agonists shift the cocaine dose effect function to the left on a fixed ratio (FR) schedule and increase cocaine intake on a PR schedule, suggesting that 5-HT1B renhances enhancocaineine reinforcement and motivation for cocaine.
The attenuating effects of CP 94,253 on the descending limb of the cocaine dose effect function were blocked by the selective 5-HT1B receptor antagonist SB 224289 (5 mg/kg, i.p). at both time points, indicating 5-HT1B receptor mediation.
The effects of CP 94,253 on the descending limb of the cocaine dose effect function were blocked by the selective 5-HT1B receptor antagonist SB 224289 (5.0 mg/kg, i.p ., which produced no discernible effects on its own, suggesting that stimulation of 5-HT1B renhances enhances the reinforcing effects of cocaine during maintenance.
