Synaptically activated Ca2+ waves and NMDA spikes locally suppress voltage-dependent Ca2+ signalling in rat pyramidal cell dendrites

摘要

Non-technical summarySynaptically activated changes in dendritic [Ca²⁺]i affect many important physiological processes including synaptic plasticity and gene expression. The location, magnitude and time course of these changes can determine which mechanisms are affected. Therefore, it is important to understand the processes that control and modulate these changes. One important source is Ca²⁺ entering through voltage-gated Ca²⁺ channels opened by action potentials backpropagating over the dendrites (bAPs). Here we examine how [Ca²⁺]i changes, caused by regenerative Ca²⁺ release from internal stores (Ca²⁺ waves) or by regenerative Ca²⁺ entry through NMDA receptors (NMDA spikes), affect subsequent bAP-evoked [Ca²⁺]i changes. These large [Ca²⁺]i increases suppressed the bAP signals in the regions where the preceding [Ca²⁺]i increases were largest. The suppression was proportional to the magnitude of the large [Ca²⁺]i change and was insensitive to kinase and phosphatase inhibitors, consistent with suppression due to Ca²⁺-dependent inhibition of Ca²⁺ channels.