Journal
NEURON
Volume 33, Issue 3, Pages 439-452Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(02)00573-1
Keywords
-
Categories
Ask authors/readers for more resources
Spine Ca2+ is critical for the induction of synaptic plasticity, but the factors that control Ca2+ handling in dendritic spines under physiological conditions are largely unknown. We studied [Ca2+] signaling in dendritic spines of CA1 pyramidal neurons and find that spines are specialized structures with low endogenous Ca2+ buffer capacity that allows large and extremely rapid [Ca2+] changes. Under physiological conditions, Ca2+ diffusion across the spine neck is negligible, and the spine head functions as a separate compartment on long time scales, allowing localized Ca2+ buildup during trains of synaptic stimuli. Furthermore, the kinetics of Ca2+ sources governs the time course of [Ca2+] signals and may explain the selective activation of long-term synaptic potentiation (LTP) and long-term depression (LTD) by NMDA-R-mediated synaptic Ca2+.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available