Effects of ibogaine on naloxone-precipitated withdrawal in morphine-dependent mice.
B Francés, R Gout, J Cros, J M Zajac
Fundamental & clinical pharmacology January 1, 1992 DOI: 10.1111/j.1472-8206.1992.tb00127.x
Summary
Ibogaine, at a dose of 30 mg/kg, enhanced morphine's pain-relieving effects in naive mice but did not relieve withdrawal symptoms in morphine-dependent mice. Instead, it increased naloxone-induced vertical jumps by 68%, regardless of chronic morphine treatment length. In contrast, a non-convulsant drug, alpha-napthoxyacetic acid, did not show significant changes when combined with ibogaine. These findings suggest that while ibogaine influences morphine's effectiveness against pain, it does not alleviate opioid withdrawal symptoms in mice.
Abstract
In naive mice, ibogaine at a tremorigenic dose (30 mg/kg, ip), did not produce antinociception but did potentiate the antinociceptive potency of morphine in the tail-flick test. In morphine-dependent mice, ibogaine did not eliminate withdrawal symptoms but significantly increased the number of repetitive vertical jumps induced by naloxone, whatever the duration of the chronic morphine treatment. By comparison, repetitive jumping induced by alpha-napthoxyacetic acid (alpha-NOAA), a non-convulsant drug which induced jumping without affecting other morphine-withdrawal signs, was not significantly modified by ibogaine. These results indicate that while acute antinociceptive effects of morphine are modulated by ibogaine, this drug, shown to alleviate opiate dependence in man, does not attenuate in mice opioid withdrawal manifestations.