Dendritic spine formation and pruning: common cellular mechanisms?
The recent advent of novel high-resolution imaging methods has created a flurry of exciting observations that address a century-old question: what are biological signals that regulate formation and elimination of dendritic spines? 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 structure that can undergo fast morphological variations. Recent conflicting reports on the regulation of spine morphology lead to the proposal of a unifying hypothesis for a common mechanism involving changes in postsynaptic intracellular Ca2+ concentration, [Ca2+]i: a moderate rise in [Ca2+]i causes elongation of dendritic spines, while a very large increase in [Ca2+]i causes fast shrinkage and eventual collapse of spines. This hypothesis provides a parsimonious explanation for conflicting reports on activity-dependent changes in dendritic spine morphology, and might link these changes to functional plasticity in central neurons.
Segal
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Dept of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel.
Korkotian
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Murphy
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D000818:Animals; D002118:Calcium / Q000378:metabolism; D018929:Cell Culture Techniques; D048429:Cell Size; D003712:Dendrites / Q000378:metabolism*; D006801:Humans; D008954:Models, Biological; D009473:Neuronal Plasticity; D015398:Signal Transduction
D002118:Calcium