Cocaine dependence ibogaine

Ibogaine itself stimulates locomotor activity in rats. However, it reduces the locomotor activity induced by morphine, with greater effects in female animals than males (Pearl et al. 1997). It also reduces locomotor activity induced by cocaine and amphetamine (Sershen et al. 1992a, 1992b Blackburn and Szumlinski 1997). However, the interaction between ibogaine and cocaine is time-dependent, with motor activity inhibited at short delays, but potentiated at long delays (Maisonneuve et al. 1997). 

Until the mid-1980s ibogaine had no apparent therapeutic value. Interest was stimulated with the filing of a patent for ibogaine treatment of opiate dependence. Four other patent filings followed in rapid succession for treatment of cocaine, amphetamine, alcohol and nicotine/ tobacco dependence syndromes 8,2). Current research has focused on 18-methoxycoronaridine, a synthetic derivative of ibogaine 104-106). 

Beginning in 1985, a series of patents was issued for the use of ibogaine as a rapid means of interrupting addiction to narcotics (morphine and heroin) (3), cocaine and amphetamine (4), alcohol (5), nicotine (6) and polydrug dependency syndrome (35). These patents claim that an oral or rectal dose of ibogaine (4-25 mg/kg) interrupts the dependence syndrome, allowing patients to maintain a drug-free lifestyle for at least 6 months. 

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