Effects of ibogaine on naloxone-precipitated withdrawal in morphine-dependent mice.
B Francés, R Gout, J Cros, J M Zajac
Fundamental & clinical pharmacology 1992 DOI: 10.1111/j.1472-8206.1992.tb00127.x (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Naive and morphine-dependent mice |
| Interventions | Ibogaine morphine naloxone alpha-napthoxyacetic acid |
| Dose | 30 mg/kg |
| Topics | Ibogaine |
| Citations | 46 |
| Key findings | Ibogaine potentiated morphine's antinociceptive effect but did not attenuate opioid withdrawal manifestations 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.