Blockage of Ca2+ uptake with thapsigargin, a specific antagonist of sarco/endoplasmic reticulum Ca2+-ATPase pumps, causes an increase of somatic Ca2+, with negligible changes of Ca2+ levels in dendrites. Treatment with thapsigargin in the presence of blockers of NMDA (N-methyl-D-aspartic acid) receptors upregulates some activity-dependent genes (Egr2 and Nr4a1), leaving unaltered the expression level of other activity-dependent genes (Bdnf and Arc). These results show that the elevation of somatic Ca2+ can initiate transcription of specific genes, independently of activation of NMDA receptors, but that transcription of other genes is not initiated by a simple elevation of intracellular Ca2+.
