CALCIUM HOMEOSTASIS IN AGED NEURONS

Mechanisms of cytoplasmic calcium homeostasis were investigated in per ipheral and central neurones isolated from neonatal, adult and old Wis tar rats and in granule neurones in acutely prepared cerebellar slices of adult and old CBA mice. The cytoplasmic calcium concentration ([Ca 2+](i)) was measured by either indo-1- or fura-2-based microfluorimetr y. The resting [Ca2+](i) was significantly higher in senile neurones. The depolarization-induced [Ca2+](i) transients were markedly altered in old neurones when compared with adult ones: the age-associated chan ges in stimulus-evoked [Ca2+](i) signalling comprised of (i) significa nt decrease of the amplitudes of [Ca2+](i) transients; (ii) prolongati on of the rising phase and (iii) prominent deceleration of the recover y of the [Ca2+](i) elevation towards the resting level after the end o f depolarization. The amplitudes of calcium release from caffeine/Ca2-sensitive endoplasmic reticulum calcium stores became significantly s maller in old central neurones, whereas they remained unaffected in pe ripheral neurones. Based on our observations we can conclude that agei ng of the nervous system is associated with significant changes in mec hanisms of [Ca2+](i) homeostasis in individual neurones. These changes lead to a stable increase in the resting [Ca2+](i) and to a substanti al prolongation of stimulus-evoked [Ca2+](i) signals. We could suggest also that the ability of the old neurones to handle Ca2+ loads is dim inished, which may determine higher vulnerability of aged neurones to excess of calcium ions.