Brief Communication Low Voltage-Activated Ca Channels Are Coupled to Ca - Induced Ca Release in Rat Thalamic Midline Neurons

High voltage-activated Ca 2 channels are coupled to the release of Ca 2 from intracellular stores. Here we present evidence that, in the paraventricular thalamic nucleus and other midline thalamic nuclei, activation of low voltage-activated (LVA) Ca 2 channels stimulates Ca 2 -induced Ca 2 release (CICR) from intracellular stores. Voltage-clamp activation of LVA Ca 2 channels in fluo-4 AM-loaded neurons induced an initial transient increase in intracellular Ca 2 concentrations ([Ca 2 ]i ) (mean increase, 19.4%; decay time constant, 71 ms) that reflected the entry of extracellular Ca 2 . This was followed by a sustained secondary elevation in [Ca 2 ]i (mean increase, 4.7%; decay time constant, 7310 ms) that was attributable to CICR. Repeated activation of LVA Ca 2 channels to evoke CICR caused a progressive buildup of baseline [Ca 2 ]i (mean increase, 13.12 3.41%) that was reduced by depletion of intracellular Ca 2 stores with thapsigargin or caffeine. In contrast, LVA Ca 2 channel-evoked CICR was absent from ventrolateral thalamocortical relay neurons, suggesting that LVA Ca 2 channel coupling to Ca 2 -dependent intracellular signaling may be a property that is unique to nonspecific and midline thalamocortical neurons.