Journal
JOURNAL OF NEUROSCIENCE
Volume 25, Issue 36, Pages 8267-8271Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1942-05.2005
Keywords
calcium; thalamus; phasic; Ca2+-induced Ca2+ release; imaging; neuron
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High voltage-activated Ca2+ channels are coupled to the release of Ca2+ from intracellular stores. Here we present evidence that, in the paraventricular thalamic nucleus and other midline thalamic nuclei, activation of low voltage-activated (LVA) Ca2+ channels stimulates Ca2+- induced Ca2+ release (CICR) from intracellular stores. Voltage-clamp activation of LVA Ca2+ channels in fluo-4 AM-loaded neurons induced an initial transient increase in intracellular Ca2+ concentrations ([Ca2+](i)) ( mean increase, 19.4%; decay time constant, 71 ms) that reflected the entry of extracellular Ca2+. This was followed by a sustained secondary elevation in [Ca2+](i) ( mean increase, 4.7%; decay time constant, 7310 ms) that was attributable to CICR. Repeated activation of LVA Ca2+ channels to evoke CICR caused a progressive buildup of baseline [Ca2+](i) ( mean increase, 13.12 +/- 3.41%) that was reduced by depletion of intracellular Ca2+ stores with thapsigargin or caffeine. In contrast, LVA Ca2+ channel-evoked CICR was absent from ventrolateral thalamocortical relay neurons, suggesting that LVA Ca2+ channel coupling to Ca2+-dependent intracellular signaling may be a property that is unique to nonspecific and midline thalamocortical neurons.
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