Excitotoxic insult due to ibogaine leads to delayed induction of neuronal NOS in Purkinje cells.
Neuroreport – August 21, 1995
Source: PubMed
Summary
Ibogaine leads to degeneration of Purkinje cells, with notable effects observed in 100% of treated subjects. After administration, some Purkinje cells began expressing NADPH-diaphorase and neuronal nitric oxide synthase (nNOS), which are normally absent. The induction of nNOS was dose-related and delayed, particularly in neurons near damaged Purkinje cells. These findings suggest that while nitric oxide may not be involved in the initial damage, it could play a role 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.