Effects of ibogaine on responding maintained by food, cocaine and heroin reinforcement in rats

Abstract

The effects of ibogaine (40 and 80 mg/kg, i.p.), an indole alkaloid proposed for the treatment of drug abuse, were determined in three different groups of rats responding under an FR10 schedule of food, cocaine or heroin reinforcement. Ibogaine (80 mg/kg, i.p.) given 60 min before the start of the session resulted in a 97% decrease in the number of ratios completed under the food reinforcement schedule and resulted in a decrease in responding the following day. Neither 40 mg/kg ibogaine given 60 min prior to the session nor 80 mg/kg given 24 h before the session suppressed responding maintained by cocaine infusions (0.33 mg/infusion). Pretreatment with 80 mg/kg ibogaine either 60 or 90 min prior to the session suppressed cocaine self-administration on the day it was administered and the longer pretreatment continued to suppress responding for 48 h. Responding maintained by heroin (18 micrograms/infusion) was the most sensitive to the effects of ibogaine. Both 40 and 80 mg/kg ibogaine resulted in an almost complete suppression of responding following a 60-min pretreatment period. Responding maintained by heroin returned to control levels the day following the administration of ibogaine.

Glial Cell Line-Derived Neurotrophic Factor Mediates the Desirable Actions of the Anti-Addiction Drug Ibogaine against Alcohol Consumption

“…Systemic injections were intraperitoneal and given in injection volumes of 2 ml/kg for rats and 1 ml/100 gm for mice at a concentration of 20 or 40 mg/kg. The 40 mg/kg dose of ibogaine has been reported previously to reduce cocaine and heroin self-administration (Glick et al, 1992;Cappendijk and Dzoljic, 1993;Dworkin et al, 1995). This dose of ibogaine is not toxic to cells because it was shown not to produce Purkinje cell death (Molinari et al, 1996).…”

“…The 40 mg/kg dose was chosen because it has been reported to reduce cocaine and heroin self-administration (Glick et al, 1992;Cappendijk and Dzoljic, 1993;Dworkin et al, 1995) without evidence of neurotoxicity (Molinari et al, 1996). Under conditions of continuous access to ethanol in the home cage, the acute administration of ibogaine reduced both intake of (Fig.…”

“…Studies also suggest that ibogaine attenuates drug-and ethanolinduced behaviors in rodents. For example, ibogaine reduces operant self-administration of heroin in rats, as well as naloxoneprecipitated withdrawal in morphine-dependent rats (Glick et al, 1992;Dworkin et al, 1995). Administration of ibogaine decreases cocaine-induced locomotor activity and reduces cocaine self-administration in rats (Cappendijk and Dzoljic, 1993) and mice (Sershen et al, 1994).…”

Neurochemical and behavioural interactions between ibogaine and nicotine in the rat

“…Recently, it has been reported (Cappendjik & Dzol ic, 1993;Dworkin et al, 1995;Popik et al, 1995) that U.S. patents have been awarded to Howard Lotsof (1985, 1986, 1989 for the use of ibogaine as an anti-addictive agent in the treatment of opiate (Patent No. 4,499,096) and stimulant abuse (Patent No.…”

“…The evidence available suggests that ibogaine can attenuate the self-administration of opiates (Glick et al, 1991;Dworkin et al, 1995) and cocaine (Cappendjik & Dzoljic, 1993;Dworkin et al, 1995) by rats. Further support for the possible effectiveness of this alkaloid, at least in the treatment of opiate abuse, comes from the reports that morphine-evoked increases in nucleus accumbens dopamine overflow and locomotor activity are blocked by ibogaine-pretreatment (Maisonneuve et al, 1991) and that some, though not all, of the naloxoneprecipitated withdrawal symptoms are relieved following ibogaine (Dzoljic et al, 1988;Glick et al, 1992).…”