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

E O'Hearn, P Zhang, M E Molliver

Neuroreport August 21, 1995 DOI: 10.1097/00001756-199508000-00006 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Experimental study Peer reviewed
Population Purkinje cells in the brain
Intervention Ibogaine
Topics Ibogaine
Citations 77
Key findings Ibogaine induces delayed expression of nNOS in Purkinje cells adjacent to degenerated ones, suggesting NO may be involved in recovery or delayed cell death after excitotoxic injury.

Abstract

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 detected in neurons adjacent to degenerated PKCs. The results demonstrate that nNOS induction can follow excitotoxic neuronal injury or perturbation. However, NO is unlikely to participate in the initial phase of PKC damage. Both the late induction of nNOS and the spatial relationship between damaged and nNOS-expressing PKCs are consistent with a role for NO in either neuronal recovery or delayed cell death following excitotoxic injury.

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