Neuronal plasticity is a key issue in neuroscience. It is defined as the capability of the neuron to adapt to a changing internal or external environment, to previous experience or to trauma. It appears that during all phases of the individual life span in the nervous system, changes take place that relate to development, degeneration, and regeneration. Growth cones are a focus of neuronal plasticity, and current views emphasize the importance of local intracellular [Ca2+] to the control of their function. Hence, outgrowth of neurites from neurons in culture may be manipulated by drugs that affect intracellular Ca2+ homeostasis. In the adult nervous system, much research deals with synaptic plasticity, especially with the activity-dependent changes seen after long-term potentation of hippocampal synapses. As in the growth cone, such changes involve Ca(2+)-dependent pre- and postsynaptic processes, among which is the activation of protein kinase C. During aging, Ca2+ homeostasis may be slightly disturbed over a long period of time that could result in loss of function seen after a short, toxic high level of intracellular [Ca2+]. In this respect, the beneficial effects of chronic treatment with the L-channel Ca(2+)-blocker nimodipine on sensorimotor function of aged rats is discussed.