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The Journal of Neuroscience, September 7, 2005, 25(36):8267-8271; doi:10.1523/JNEUROSCI.1942-05.2005

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Low Voltage-Activated Ca²⁺ Channels Are Coupled to Ca²⁺-Induced Ca²⁺ Release in Rat Thalamic Midline Neurons

Trevor A. Richter, Miloslav Kolaj, and Leo P. Renaud

Neurosciences, Ottawa Health Research Institute, Ottawa, Ontario, Canada K1Y 4E9

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.

Key words: calcium; thalamus; phasic; Ca²⁺-induced Ca²⁺ release; imaging; neuron

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Received May 16, 2005; revised July 26, 2005; accepted July 27, 2005.

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