The neuroprotective effects of (-)deprenyl in the gerbil hippocampus following transient global ischemia.

Abstract

(-)Deprenyl (selegeline) is a monoamine oxidase B (MAO-B) inhibitor, but it also exerts several effects independent of MAO-B inhibition. For example, it has been shown to improve neuronal survival in different neurodegenerative models. In the present study, we have tested whether (-)deprenyl attenuates the neuronal damage in the hippocampus that is induced in a model of transient global ischemia in gerbils. (-)Deprenyl was administered 1) at a low daily dose starting two weeks before occlusion, 2) at a single high dose administered 3h after occlusion, or 3) at a low daily dose for one or two weeks after occlusion. A nonsignificant trend of reduced neuronal damage in the hippocampal CA1 area was seen in all experimental groups treated with (-)deprenyl, regardless of the timing of treatment. The results together with previous evidence suggest that (-)deprenyl may protect CA1 neurons from ischemia-induced delayed death by several possible mechanisms, including the suppression of oxidative stress and apoptotic processes.

• Authors: J Kuhmonen, J Jolkkonen, A Haapalinna, J Sivenius
• Journal: Journal of neural transmission (Vienna, Austria : 1996) (J Neural Transm (Vienna)) Vol. 107 Issue 7 Pg. 779-86 ( 2000) ISSN: 0300-9564 [Print] Austria
• PMID: 11005543 (Publication Type: Journal Article)

Chemical References

• Monoamine Oxidase Inhibitors
• Selegiline

Topics

• Animals
• Brain Ischemia (drug therapy, pathology)
• Cell Death (drug effects, physiology)
• Female
• Gerbillinae
• Hippocampus (blood supply, drug effects, pathology)
• Monoamine Oxidase Inhibitors (pharmacology, therapeutic use)
• Pyramidal Cells (drug effects, pathology)
• Selegiline (pharmacology, therapeutic use)