The Life Cycle of Ca2 Ions in Dendritic Spines

specificity in synaptic plasticity (Andersen et al., 1980). Spine [Ca2] signals are shaped by the dynamics of Ca2 sources and extrusion mechanisms, the propertiesSummary and spatial distribution of Ca2 buffers, and diffusion between dendrite and spine (reviewed in Sabatini et al.Spine Ca2 is critical for the induction of synaptic plas-[2001]). Using high-resolution imaging techniques, theticity, but the factors that control Ca2 handling in den-sources of spine [Ca2] have been explored under adritic spines under physiological conditions are largely variety of stimulation conditions. In pyramidal neurons,unknown. We studied [Ca2] signaling in dendritic weak synaptic activation leads to postsynaptic Ca2 in-spines of CA1 pyramidal neurons and find that spines flux primarily through NMDA-Rs (Koester and Sakmann,are specialized structures with low endogenous Ca2 1998; Kovalchuk et al., 2000; Yuste et al., 1999). Supra-buffer capacity that allows large and extremely rapid threshold stimuli produce additional Ca2 influx through[Ca2] changes. Under physiological conditions, Ca2 VSCCs opened by backpropagating action potentialsdiffusion across the spine neck is negligible, and the (Jaffe et al., 1992; Majewska et al., 2000b; Sabatini andspine head functions as a separate compartment on Svoboda, 2000; Yuste and Denk, 1995). Under somelong time scales, allowing localized Ca2 buildup dur