ubiquinone and 1-3-butylene-glycol

We previously showed that intrastriatal administration of aminooxyacetic acid (AOAA) produces striatal lesions by a secondary excitotoxic mechanism associated with impairment of oxidative phosphorylation. In the present study, we show that and the specific complex I inhibitor rotenone produces a similar neurochemical profile in the striatum, consistent with an effect of AOAA on energy metabolism. Lesions produced by AOAA were dose-dependently blocked by MK-801, with complete protection against GABA and substance P depletions at a dose of 3 mg/kg. AOAA lesions were significantly attenuated by pretreatment with either 1,3-butanediol or coenzyme Q10, two compounds which are thought to improve energy metabolism. These results provide further evidence that AOAA produces striatal excitotoxic lesions as a consequence of energy depletion and they suggest therapeutic strategies which may be useful in neurodegenerative diseases.

Topics: Aminooxyacetic Acid; Animals; Aspartic Acid; Butylene Glycols; Coenzymes; Corpus Striatum; Dizocilpine Maleate; Ketone Bodies; Malates; Male; Mitochondria; NAD(P)H Dehydrogenase (Quinone); Neurotransmitter Agents; Oxidative Phosphorylation; Rats; Rats, Sprague-Dawley; Rotenone; Ubiquinone