Effects of ibogaine on naloxone-precipitated withdrawal in morphine-dependent mice.

In mice, a tremor-inducing dose of ibogaine did not relieve pain on its own but made morphine more effective at relieving pain. In morphine-dependent mice, ibogaine did not reduce withdrawal symptoms; instead, it increased the number of vertical jumps caused by naloxone, a drug that triggers withdrawal. This effect was specific to opioid withdrawal, as ibogaine did not alter jumping caused by a different drug. The results indicate that ibogaine modulates morphine's pain-relieving effects but does not lessen opioid withdrawal signs in mice, contrasting with reports of it alleviating opiate dependence in humans.

Study at a glance

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.