Résumé
Excitation-transcription coupling makes use of cellular excitability to produce intracellular signals to the nucleus to control activity-dependent gene expression. Voltage-gated calcium channels are presented here as a signaling platform able to redirect multiple signaling pathways toward the nucleus. Whilst several CaV subunits are implicated in excitation-transcription coupling, each type of CaV nevertheless possesses its own proteome and microenvironment able to promote individualized signaling pathways. L-type calcium channels have structural determinants that favor the initiation of MAPK and CamK pathways for example, but P/Q and N-type channels, in close proximity to the endoplasmic reticulum, promote calcium-induced calcium release-dependent mechanisms. Furthermore, auxiliary CaVβ4 subunits or truncated C-termini of CaV1.2 and CaV2.1 channels can be targeted to the nucleus and become direct messengers involved in the regulation of gene expression. These later discoveries suggest that novel pathways must be inserted in the global description of excitation-transcription coupling and give new clues to the understanding of calcium channelopathies with interesting physiopathological perspectives.