Iboga compounds reverse the behavioural disinhibiting and corticosterone effects of acute methamphetamine: Implications for their antiaddictive properties.
Karen K. Szumlinski, R E Haskew, M Y Balogun, Isabelle M Maisonneuve, Stanley D Glick
Pharmacology, biochemistry, and behavior 2001 DOI: 10.1016/s0091-3057(01)00564-0 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Randomized controlled trial Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | Ibogaine 18-methoxycoronaridine |
| Dose | 40 mg/kg ip |
| Duration | 19-hour pretreatment, acute methamphetamine administration 20 minutes before testing |
| Topics | Ibogaine |
| Keywords | Iboga compounds Ibogaine derivatives Iboga alkaloids Stimulant addiction treatment Drug addiction therapy Substance abuse treatment Anti-addiction potential Stimulant reversal Methamphetamine treatment Neuropharmacology Psychopharmacology Behavioral neuroscience Stress response modulation Drug mechanisms Crystal meth |
| Citations | 28 |
| Key findings | Ibogaine and 18-methoxycoronaridine antagonized the behavioral disinhibition and corticosterone increase induced by methamphetamine. |
Abstract
This study investigated the effects of pretreatment with the putative antiaddictive compound, ibogaine (IBO), and its synthetic derivative, 18-methoxycoronaridine (18-MC), on the changes in behaviour in an elevated plus maze and the changes in corticosterone (CORT) produced by a low dose of methamphetamine (METH). In the elevated plus maze, the acute administration of METH (0.1 mg/kg ip, -20 min) produced an increase in both the number and the duration of open arm entries relative to saline (SAL)-treated controls. No effect of METH administration was observed on the total number of arm entries. These data indicated that METH alone produced either anxiolysis or behavioural disinhibition in this paradigm. More consistent with the latter possibility, the open arm behaviour of METH controls was associated with an increase in plasma levels of CORT, supporting a facilitatory role for CORT in this METH-induced effect. Pretreatment with both IBO and 18-MC (40 mg/kg ip, 19 h earlier) antagonized the behavioural disinhibiting effects of acute METH without altering locomotor activity. In addition, both iboga agents antagonized the increase in CORT produced by METH. These data provide insight into yet another potential mechanism through which iboga compounds may exert their antiaddictive effects, a reversal of the behavioural disinhibiting properties of stimulant drugs. Furthermore, these data indicate that this reversal is related to effects of iboga compounds on the stimulation of neuroendocrine systems by stimulant drugs.