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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Spino-dendritic cross-talk in rodent Purkinje neurons mediated by endogenous Ca2+-binding proteins.

The range of actions of the second messenger Ca(2+) is a key determinant of neuronal excitability and plasticity. For dendritic spines, there is on-going debate regarding how diffusional efflux of Ca(2+) affects spine signalling. However, the consequences of spino-dendritic coupling for dendritic Ca(2+) homeostasis and downstream signalling cascades have not been explored to date. We addressed this question by four-dimensional computer simulations, which were based on Ca(2+)-imaging data from mice that either express or lack distinct endogenous Ca(2+)-binding proteins. Our simulations revealed that single active spines do not affect dendritic Ca(2+) signalling. Neighbouring, coactive spines, however, induce sizeable increases in dendritic [Ca(2+)](i) when they process slow synaptic Ca(2+) signals, such as those implicated in the induction of long-term plasticity. This spino-dendritic coupling is mediated by buffered diffusion, specifically by diffusing calbindin-bound Ca(2+). This represents a central mechanism for activating calmodulin in dendritic shafts and therefore a novel form of signal integration in spiny dendrites.[1]

References

  1. Spino-dendritic cross-talk in rodent Purkinje neurons mediated by endogenous Ca2+-binding proteins. Schmidt, H., Kunerth, S., Wilms, C., Strotmann, R., Eilers, J. J. Physiol. (Lond.) (2007) [Pubmed]
 
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