Mechanisms of cytoplasmic calcium homeostasis were investigated in peripheral and central neurones isolated from neonatal, adult and old Wistar rats and in granule neurones in acutely prepared cerebellar slices of adult and old CBA mice. The cytoplasmic calcium concentration ([Ca2+](i)) was measured by either indo-1- or fura-2-based microfluorimetry. 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 changes in stimulus-evoked [Ca2+](i) signalling comprised of (i) significant decrease of the amplitudes of [Ca2+](i) transients; (ii) prolongation of the rising phase and (iii) prominent deceleration of the recovery of the [Ca2+](i) elevation towards the resting level after the end of depolarization. The amplitudes of calcium release from caffeine/Ca2+-sensitive endoplasmic reticulum calcium stores became significantly smaller in old central neurones, whereas they remained unaffected in peripheral neurones. Based on our observations we can conclude that ageing of the nervous system is associated with significant changes in mechanisms of [Ca2+](i) homeostasis in individual neurones. These changes lead to a stable increase in the resting [Ca2+](i) and to a substantial prolongation of stimulus-evoked [Ca2+](i) signals. We could suggest also that the ability of the old neurones to handle Ca2+ loads is diminished, which may determine higher vulnerability of aged neurones to excess of calcium ions.
- brain slices
- Calcium aging