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

  title={Degeneration of purkinje cells in parasagittal zones of the cerebellar vermis after treatment with ibogaine or harmaline},
  author={Elizabeth O'hearn and Mark E. Molliver},

The Olivocerebellar Projection Mediates Ibogaine-Induced Degeneration of Purkinje Cells: A Model of Indirect, Trans-Synaptic Excitotoxicity

The results show that ibogaine administered after inferior olive ablation produced little or no Purkinje cell degeneration or glial activation, and that a lesion of the inferior olive almost completely prevents the neurotoxicity, demonstrating that Ibogaine is not directly toxic toPurkinje cells, but that the toxicity is indirect and dependent on integrity of the olivocerebellar projection.

NOS and fos in Rat and Mouse Brain Regions

The localization of the nuclear ear lyhmedia te gene product c-fos as a biomarker of the ibogaine drug effect on cells in various brain regions, including the cerebellum, of rats compared to mice is reported to indicate the pharmacokinetics may be similar in rats and mice, although the pharmacodynamic effects of the drug on cortex may differ.

Exposure to Kainic Acid Mimics the Effects of Axotomy in Cerebellar Purkinje Cells of the Adult Rat

It is proposed that kainic acid‐induced intracellular calcium overload disrupts cytoskeletal components and impairs axonal transport, thus depriving the affected Purkinje cells of retrograde trophic influences from their target neurons, and the affected neurons undergo long‐lasting regressive modifications and compensatory remodelling phenomena.

A dose-response study of ibogaine-induced neuropathology in the rat cerebellum.

Observations affirm the usefulness of GFAP immunohistochemistry as a sensitive biomarker of neurotoxicity in cerebellar neurotoxicity and suggest this dose level may be considered as a no-observable-adverse-effect level (NOAEL).

Excitotoxic Mechanisms of Neurodegeneration in Transmissible Spongiform Encephalopathies

Close similarity in the appearance, localization, and functional consequences from TSE neuropathology compared to some of the well-known EAA syndromes implies that neuroprotective strategies against excitotoxicity may also be effective against TSEs.

The effect of memantine in harmaline-induced tremor and neurodegeneration




Ibogaine induces glial activation in parasagittal zones of the cerebellum.

The ibogaine-induced activation of cerebellar glial cells is highly suggestive of neuronal degeneration, most likely of Purkinje cells.

Axonal abnormalities in cerebellar Purkinje cells of the ‘hyperspiny Purkinje cell’ mutant mouse

The definite axonal pathology ofhpc Purkinje cells confers to this mutation its own specificity, which differs from all other known mutations primarily affecting this neuronal population.

Dual serotoninergic projections to forebrain in the rat: Morphologically distinct 5‐HT axon terminals exhibit differential vulnerability to neurotoxic amphetamine derivatives

It is demonstrated that the two axon types differ markedly in their vulnerability to the neurotoxic amphetamine derivatives, methylenedioxyamphetamine (MDA), and p‐chloroamphetamine (PCA), and that beaded 5‐HT axons are consistently spared.

Effect of Climbing Fiber Deprivation on Release of Endogenous Aspartate, Glutamate, and Homocysteate in Slices of Rat Cerebellar Hemispheres and Vermis

The hypothesis that Asp is a transmitter candidate of the climbing fibers projecting to the cerebellar hemispheres, but not to the vermis is supported, and the first evidence that HCA can be linked to a specific pathway is provided.

Electrophysiological properties of in vitro Purkinje cell dendrites in mammalian cerebellar slices.

1. Intradendritic recordings from Purkinje cells in vitro indicate that white matter stimulation produces large synaptic responses by the activation of the climbing fibre afferent, but antidromic

Mechanisms of AMPA Neurotoxicity in Rat Brain Slices

The results indicate that the rapid oedematous necrosis induced by AMPA, like that caused by N‐methyl‐d‐aspartate and kainate, is likely to involve excessive influx of Ca2+.