Hemodynamic, Metabolic, Ionic, and Electrical Responses to Cortical Spreading Depression in Aging Rats

Abstract

Spreading depression (SD) is a phenomenon that has been described in the literature as depression of spontaneous electrical activity (Leao, 1944). It is accompanied by increased metabolic activity (Rosenthal and Somjen, 1973; Mayevsky and Chance, 1974; Hansen et al., 1980), changes in cerebral blood flow (Shibata et al., 1990; Piper et al., 1991) and fluctuations in ionic homeostasis (Hansen and Zeuthen, 1981; Mayevsky et al, 1982). Previous results from our laboratory indicate that the nature of the response to spreading depression is dependent on the ability of the brain to compensate for extra oxygen needed by increasing blood flow to the activated site (Mayevsky et al., 1982; Mayevsky and Weiss, 1991). It was also found that this ability of the brain is age-dependent, namely, adult brain showed “oxidation cycles” of the NADH in most conditions, while the young rat and the anesthetized gerbil brains exhibited “reduction cycle” of the NADH. On the other hand other studies demonstrated that aging acts intracellularly to limit the brain’s capacity to increase oxidative phosphorylation to meet heightened ATP damage (Benzi et al., 1992). Furthermore, it is also already known that the metabolic functions of the brain as well as its blood supply inevitably decline with age (Meyer et al., 1993).