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M E Molliver

4 papers in the library · 385 citations · publishing 1993-2004

Papers

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Administration of a non-NMDA antagonist, GYKI 52466, increases excitotoxic Purkinje cell degeneration caused by ibogaine.

Neuroscience 2004 E O'Hearn, M E Molliver 16 citations

Ibogaine is a tremorigenic hallucinogen that has been proposed for clinical use in treating addiction. We previously reported that ibogaine, administered systemically, produces degeneration of a subset of Purkinje cells in the cerebellum, primarily within the vermis. Ablation of the inferior olive affords protection against ibogaine-induced neurotoxicity leading to the interpretation that...

Excitotoxic insult due to ibogaine leads to delayed induction of neuronal NOS in Purkinje cells.

Neuroreport August 21, 1995 E O'Hearn, P Zhang, M E Molliver 77 citations

Ibogaine causes degeneration of Purkinje cells (PKCs), presumably via activation of neurons in the inferior olive leading to release of glutamate at climbing fiber terminals. Following ibogaine administration, some Purkinje cells express NADPH-diaphorase and neuronal NOS (nNOS), neither of which is present normally in these cells. The induction of NOS is delayed in onset, dose-related, and...

Degeneration of Purkinje cells in parasagittal zones of the cerebellar vermis after treatment with ibogaine or harmaline.

Neuroscience July 1, 1993 E O'Hearn, M E Molliver 220 citations

The indole alkaloids ibogaine and harmaline are beta-carboline derivatives that cause both hallucinations and tremor. Reports that ibogaine may have potent anti-addictive properties have led to initiatives that it be tested for the treatment of opiate and cocaine addiction. In this study, ibogaine-treated rats were analysed for evidence of neurotoxic effects because human clinical trials of...

Ibogaine induces glial activation in parasagittal zones of the cerebellum.

Neuroreport March 1, 1993 E O'Hearn, D B Long, M E Molliver 72 citations

Ibogaine, an indole alkaloid, has been proposed for treatment of drug addiction, yet its mechanism, site of action, and possible neurotoxicity have not been determined. Since neuronal injury is known to activate neurologlial cells, we investigated potential neurotoxic effects of this drug in rats by examining expression of specific glial markers. After treatment with ibogaine (100 mg kg-1 i.p.;...