Properties of ibogaine and its principal metabolite (12-hydroxyibogamine) at the MK-801 binding site of the NMDA receptor complex

Mash, Deborah C.; Staley, Julie K.; Pablo, John; Holohean, Alice M.; Hackman, J.C.; Davidoff, Robert A.

doi:10.1016/0304-3940(95)11608-y

Cited by 74 publications

(43 citation statements)

References 16 publications

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“…The K, value obtained for ibogaine (I.1 k 0.03 FM) is consistent with our previous results (Popik et al, 1994(Popik et al, . 1995a) as well as the values reported by Mash et al (1995) in human brain obtained at autopsy. The putative ibogaine metabolite O-desmethylibogaine (l2-hydroxyibogamine) [Mash et al, 1995;Pearl et al.…”

Section: Resultssupporting

confidence: 74%

“…1995a) as well as the values reported by Mash et al (1995) in human brain obtained at autopsy. The putative ibogaine metabolite O-desmethylibogaine (l2-hydroxyibogamine) [Mash et al, 1995;Pearl et al. 19951, and the chemically related iboga alkaloids ( + bogamine, ( It )coronaridine and tabemanthine were N 5-IO-fold less potent than the parent alkaloid (Table I).…”

Section: Resultssupporting

confidence: 74%

“…1995 withdrawal phenomena associated with a number of abused substances including cocaine and morphine (for review, see Popik et al, 1995b). While the nemochemical bases for the these putative 'anti-addictive' actions of ibogaine remain unclear, several recent reports (Mash et al, 1995;Popik et al, 1994, 1995a: Sweetnam et al, 1995 have shown that at pharmacologically relevant concentrations. ibogaine acts as an NMDA receptor antagonist.…”

Section: Introductionmentioning

confidence: 99%

“…ibogaine acts as an NMDA receptor antagonist. Thus, ibogaine competitively inhibits C+ )-13-3H&methyf-10,1 lw&S#f-dibenzo-[a,dIcyclohepten-5, lO-imine u 3 H]MK-801) and [piperidyl-3,4-3 H( N >I-( N-(1 -(2thienyl)cyclohexyl)-3,4-piperidine) ([ 3HJTCP) binding to NMDA receptors (Mash et al, 1995;Popik et a~. 1994Popik et a~.…”

Section: Introductionmentioning

confidence: 99%

“…, 1995aSweetnam et al, 1995). blocks glutamate-induced cell death (Popik et al, 1995a), and produces a voltage-dependent block of NMDA currents (Mash et al, 1995;Popik et al. 199Sa).…”

Section: Introductionmentioning

confidence: 99%

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Structurally modified ibogaine analogs exhibit differing affinities for NMDA receptors

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Skolnick

Bertha

et al. 1996

European Journal of Pharmacology

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Based on both preclinical findings and anecdotal evidence in man. the psychoactive indole alkaloid ihogaine has been suggested to have anti-addictive properties. Previous studies indicate that blockade of NMDA receptors may mediate at least some of the putative anti-addictive actions of ibogaine. The potencies of a series of ibogaine analogs to inhibit (+ )- attenuated naloxone precipitated withdrawal jumping. These findings are consistent with the hypothesis that inhibition of the expression of morphine dependence by ibogaine is related to its NMDA receptor antagonist properties.kWords:

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Section: Resultssupporting

confidence: 74%

Section: Resultssupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…, 1995aSweetnam et al, 1995). blocks glutamate-induced cell death (Popik et al, 1995a), and produces a voltage-dependent block of NMDA currents (Mash et al, 1995;Popik et al. 199Sa).…”

Section: Introductionmentioning

confidence: 99%

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Structurally modified ibogaine analogs exhibit differing affinities for NMDA receptors

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Skolnick

Bertha

et al. 1996

European Journal of Pharmacology

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Pharmacological screen for activities of 12-hydroxyibogamine: a primary metabolite of the indole alkaloid ibogaine

et al. 1996

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Ibogaine and the dopaminergic response to nicotine

et al. 1997

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There is increasing evidence that the rewarding effect of nicotine is mediated by the mesolimbic dopamine system. The first objective of this study was to examine the dopamine response to repeated i.v. infusions of nicotine. Using in vivo microdialysis in awake and freely moving male Sprague-Dawley rats, we demonstrated that i.v. nicotine infusions (0.16 mg/kg or 0.32 mg/kg per infusion) produced increases in extracellular dopamine levels that were dose- and infusion order-dependent. Acute tolerance was evidenced by the smaller dopamine response produced by a second infusion of nicotine, administered 1 h after the first one. Tolerance was reversible, since the dopamine response to a second infusion of nicotine was unchanged when the interval between the infusions was increased to 3 h. Ibogaine, an alkaloid found in Tabernanthe iboga, is claimed to decrease smoking and to have an anti-nicotinic action. The second objective of this study was to establish whether this claim has any neurochemical basis. Pretreatment with ibogaine (40 mg/kg, i.p.) 19 h prior to the first nicotine infusion (0.32 mg/kg per infusion) significantly attenuated the increase in extracellular dopamine levels induced by-the nicotine infusions, suggesting that ibogaine may decrease the rewarding effect of nicotine.

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Properties of ibogaine and its principal metabolite (12-hydroxyibogamine) at the MK-801 binding site of the NMDA receptor complex

Cited by 74 publications

References 16 publications

Structurally modified ibogaine analogs exhibit differing affinities for NMDA receptors

Structurally modified ibogaine analogs exhibit differing affinities for NMDA receptors

Pharmacological screen for activities of 12-hydroxyibogamine: a primary metabolite of the indole alkaloid ibogaine

Ibogaine and the dopaminergic response to nicotine

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