Chronic Int~striatal Quinolinic Acid Produces Reversible Changes in Perikaryal Calbindin and Parvalbumin Xmmunoreactivity

نویسنده

  • T. J. BAZZETT
چکیده

We recently reported the use of a chronic dialytic delivery system for intrastriatal administration of quinolinic acid in the rat.” This system produces ~~~e~ration with some characteristics simihtr to posf ntortem brain tissue from Hun~on’s disease patients, including reduced cytochrome oxidase staining, a decreased number of Nissl-stained neurons, and relative sparing of striatal NADPH-diaphorase containing neurons.’ The present findings show that chronic dialytic delivery of q~~g~c acid also produces a Huntington’s disease-like pattern of reduced caibindin and parvalbumin perikaryal hnmunoreactivity that is reversed in rats allowed four to eight weeks’ recovery after cessation of quinolinic acid. Furthermore, cytochrome oxidase staining and the number of Nissl-stained cells were unhand in the region of transient calbindin and parvalbumiu immunoreactive perikaryal staining alterations. These results suggest that changes in calbindin and parvalbumin perikaryal immunoreactivity provide a relatively sensitive measure of quinolitic acid induced ~urotoxici~. The reversible nature of reduced perikaryal immu~reactivity suggests a premorbid state of neurotoxicity, possibly marked by cellular redistribution of calbindin and parvalbumin. Quinolinic acid acts as an agonist at N-methyl-Daspartate (NMDA) receptors, causing an increase in intracellular calcium concentration.20 To maintain intracellular ionic equilibrium, calcium can be sequestered by intracellular organelles or buffered by calcium binding proteins. I3 Excessive calcium influx through the NMDA receptor complex results in excitotoxicity. 10*‘5~2’*22 Cells containing the calcium

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تاریخ انتشار 2002