Control of interneuronal communication involves a variety of homeostatic mechanisms in which free calcium ions play a fundamental role (1). An altered metabolism of calcium in the brain that occurs with aging has been observed since the beginning of this century (2). A number of data have been accumulated mostly in the last decade, indicating that aging modifies a number of functions that are strictly related to, and controlled by, calcium ions (3). Release processes, enzymatic activities, and neuronal plasticity are all impaired as a consequence of age, so that a unifying model of brain aging stressing the importance of this ion has been proposed (4).