Protection by Selegiline of Dopaminergic Neurons from Glutamate-Induced Excitotoxicity

PROTECTION BY SELEGILINE OF DOPAMINERGIC NEURONS FROM GLUTAMATE-INDUCED EXCITOTOXICITY 

The excessive activity of excitatory amino acids, such as L-glutamate and L-aspartate, followed by elevation of intracellular free Ca2+ concentration and accumulation of free radicals has been postulated to underlie the neurodegeneration that occurs after ischemic insults and trauma. Additionally, an excitotoxic component has been shown to play an important role in the pathogenesis of chronic neurodegenerative disorders, such as Alzheimer s disease, Parkinson s disease, amyotrophic lateral sclerosis, and Huntington s disease, which are characterized by progressive loss of neuronal elements. 

There is evidence from experimental Parkinson s disease models that excessive activation of NMDA receptors might be an important factor for induction of Parkinson s disease. However, the involvement of NMDA receptors has not been shown in all parkinsonian models. 

Glutathione system in loss of dopamine neurons due to impairment of energy metabolism 

Glutamate has been applied into the striatum by microdialysis, and the formation of hydroxyl radicals has been measured in the presence and absence of selegiline. In this study, microdialysis 

---