Dendritic spine formation and pruning: common cellular mechanisms?

The recent advent of novel high-resolution imaging methods has created a fl urry of exciting observations that address a century-old question: what are biological signals that regulate formation and elimination of dendritic sp ines? Contrary to the traditional belief that the spine is a stable storage site of long-term neuronal memory, the emerging picture is of a dynamic st ructure that can undergo fast morphological variations. Recent conflicting reports on the regulation of spine morphology lead to the proposal of a uni fying hypothesis for a common mechanism involving changes in postsynaptic i ntracellular Ca2+ concentration, [Ca2+](i): a moderate rise in [Ca2+](i) ca uses elongation of dendritic spines, while a very large increase in [Ca2+]( i) causes fast shrinkage and eventual collapse of spines. This hypothesis p rovides a parsimonious explanation for conflicting reports on activity-depe ndent changes in dendritic spine morphology, and might link these changes t o functional plasticity in central neurons.