Journal
NEURON
Volume 54, Issue 5, Pages 787-800Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2007.05.014
Keywords
-
Categories
Funding
- NIGMS NIH HHS [R01 GM053395-12, GM-53395, GM-65473, R01 GM053395] Funding Source: Medline
- NINDS NIH HHS [NS-34045] Funding Source: Medline
Ask authors/readers for more resources
Photolysis of a caged Ca2+ compound was used to characterize the dependence of cerebellar long-term synaptic depression (LTD) on postsynaptic Ca2+ concentration ([Ca2+](i)). Elevating [Ca2+](i) was sufficient to induce LTD without requiring any of the other signals produced by synaptic activity. A sigmoidal relationship between [Ca2+](i) and LTD indicated a highly cooperative triggering of LTD by Ca2+. The duration of the rise in [Ca2+](i) influenced the apparent Ca2+ affinity of LTD, and this time-dependent behavior could be described by a leaky integrator process with a time constant of 0.6 s. A computational model, based on a positive-feedback cycle that includes protein kinase C and MAP kinase, was capable of simulating these properties of Ca2+-triggered LTD. Disrupting this cycle experimentally also produced the predicted changes in the Ca2+ dependence of LTD. We conclude that LTD arises from a mechanism that integrates postsynaptic Ca2+ signals and that this integration may be produced by the positive-feed back cycle.
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