Low voltage-activated Ca2+ channels are coupled to Ca2+-induced Ca2+ release in rat thalamic midline neurons.
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.
Richter
Trevor A
TA
Neurosciences, Ottawa Health Research Institute, Ottawa, Ontario, K1Y 4E9, Canada.
Kolaj
Miloslav
M
Renaud
Leo P
LP
D000818:Animals; D002118:Calcium / Q000502:physiology*; D015220:Calcium Channels / Q000502:physiology*; D004558:Electric Stimulation; D066298:In Vitro Techniques; D009474:Neurons / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D051381:Rats; D017208:Rats, Wistar; D013788:Thalamus / Q000502:physiology*
D015220:Calcium Channels; D002118:Calcium