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Since their discovery at the turn of the century by Ramon y Cajal (1), dendritic spines have fascinated scientists by their unusual structure and by their likely role in cognitive functions such as learning and memory. Spines are protrusions from dendrites having diverse shapes that range more than 100-fold in size. Larger spines have proportionately larger synapses and more diversity in subcellular organelles and molecular composition than do smaller spines. These differences in spine morphology and composition might account for differences in the function of the synapses located on them. Existing data suggest that spines are maintained by optimal activation. More spines form when neurons have less excitatory activation, and spines are lost when activation is too high, or when presynaptic axons degenerate (for review, see ref. 2). This pattern suggests that neurons may homeostatically regulate input by means of the number of axospinous synapses. Recent imaging studies suggest that spines emerge or disappear depending on the age and activity of the neuron. Immature dendrites have more protrusions when the neurons have less global synaptic activation, or when there is more local activation. For example, reduced synaptic transmission results in more dendritic spines on neurons in the lateral geniculate nucleus (refs. 3 and 4; but see also ref. 5). Conversely, localized synaptic activation of cultured neurons can induce outgrowth of dendritic filopodia or spines in the vicinity of the activation (6, 7). In contrast, dendritic spines rapidly shorten and disappear from neurons exposed globally to high synaptic activity (8, 9). Mature dendrites also become increasingly spiny with a global reduction in synaptic activity (10, 11) and are lost from neurons after epileptic seizures (12). New evidence from Korkotian and Segal (13) points to release of calcium from intracellular stores as a possible modulator of dendritic …

Calcium from internal stores modifies dendritic spine shape