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P83 Regulation of [Ca2+ ]i is altered in  neurons during ischemic injury in stroke, but the precise mechanism(s)  underlying the Ca2+ dysregulation are not known. The plasma  membrane Ca2+ -ATPase (PMCA) is one of the two main  Ca2+ extrusion systems that play a critical role in  maintaining neuronal Ca2+ homeostasis. We have substantial  evidence showing that this enzyme is very sensitive to oxidative  stress. When exposed to very low concentrations of physiologically  relevant oxidants, the PMCA has been shown to form high molecular  weight aggregates and this is accompanied by the decline in its  enzymatic activity. Because stroke-induced hypoxia is associated with  the overproduction of reactive oxygen species (ROS) and a loss of  Ca2+ homeostasis, we carried out studies to determine if  the PMCA is modified in anin vivo animal model of stroke.  Global ischemia was induced in Sprague Dawley rats by occlusion of the  common carotid arteries for defined time periods. The Vmax of PMCA activity in brain homogenates as well as in purified synaptic  plasma membranes was significantly reduced following occlusion of the  vessels, and the reduction was proportional to the time of ischemia.  The loss in PMCA activity could not be reversed by addition of  exogenous ATP, suggesting an alteration in the protein itself.  Immunoblots of the synaptic membranes run under non-reducing conditions  showed crosslinking of PMCA molecules to form high molecular weight  adducts, and this too increased with increasing periods of ischemia.  The PMCA aggregates were partially reversed under reducing conditions,  indicating the involvement of sulphydryl group oxidation. These  observations support the hypothesis that increased formation of ROS  under ischemic conditions can oxidatively modify specific proteins  critical for the regulation of free [Ca2+ ]i levels. Such oxidative damage is likely to contribute to the loss of  neuronal Ca2+ regulation and neuronal viability in stroke.  (Supported by AHA 9960343Z, AG 12993, and the Higuchi Biosciences  Center, University of Kansas)

Modification of Synaptic Plasma Membrane Ca 2+ -ATPase in Ischemic Injury in an Animal Model of Global Ischemia

Modification of Synaptic Plasma Membrane Ca ²⁺ -ATPase in Ischemic Injury in an Animal Model of Global Ischemia