Skip to content

G R Hanson

3 papers in the library · 50 citations · publishing 1999-2000

Papers

Responses of the extrapyramidal and limbic substance P systems to ibogaine and cocaine treatments.

European journal of pharmacology February 25, 2000 M E Alburges, B P Ramos, L Bush et al. 21 citations

Ibogaine, a compound from the West African shrub Tabernanthe iboga, and cocaine both increased substance P—a key signaling molecule—in brain regions associated with movement and reward, specifically the striatum and substantia nigra, 12 hours after the last drug treatment. Substance P levels were not significantly raised in the nucleus accumbens by either drug. These increases were blocked by antagonists of dopamine D1 or D2 receptors, indicating involvement of dopamine pathways. Unlike cocaine, multiple doses of ibogaine did not raise substance P in the frontal cortex. The findings suggest substance P systems may contribute to the effects of ibogaine and cocaine.

Differential responses by neurotensin systems in extrapyramidal and limbic structures to ibogaine and cocaine.

Brain research February 6, 1999 M E Alburges, G R Hanson 18 citations

Ibogaine, a psychoactive compound from the West African shrub Tabernanthe iboga, increases neurotensin-like immunoreactivity (NTLI) in the striatum, nucleus accumbens, and substantia nigra of rats 12 hours after administration, but not in the frontal cortex. These increases are blocked by a D1 dopamine receptor antagonist in all three regions and by a D2 antagonist only in the substantia nigra. Ibogaine pretreatment also blocks cocaine-induced NTLI increases in the striatum and substantia nigra. The findings suggest neurotensin may mediate ibogaine's interactions with the dopamine system and contribute to its pharmacological effects against stimulant addiction.

Ibogaine pretreatment dramatically enhances the dynorphin response to cocaine.

Brain research November 13, 1999 M E Alburges, G R Hanson 11 citations

Ibogaine, a psychoactive alkaloid from the shrub Tabernanthe iboga used to treat stimulant addiction, does not by itself alter dynorphin levels in key brain regions such as the striatum, substantia nigra, or nucleus accumbens. However, when given before cocaine, ibogaine dramatically amplifies cocaine-induced increases in dynorphin content in those same structures. This suggests ibogaine may influence addiction-related brain pathways by modulating dynorphin responses to cocaine, offering insights into its anti-addiction potential.