Abstract
Recent studies have provided evidence that depolarization in the absence of extracellular Ca2+ can trigger Ca2+ release from internal stores in a variety of neuron subtypes. Here we examine whether postganglionic sympathetic neurons are able to mobilize Ca2+ from intracellular stores in response to depolarization, independent of Ca2+ influx. We measured changes in cytosolic ΔF/F0 in individual fluo-4 –loaded sympathetic ganglion neurons in response to maintained K+ depolarization in the presence (2 mM) and absence of extracellular Ca2+ ([Ca2+]e). Progressive elevations in extracellular [K+]e caused increasing membrane depolarizations that were of similar magnitude in 0 and 2 mM [Ca2+]e. Peak amplitude of ΔF/F0 transients in 2 mM [Ca2+]e increased in a linear fashion as the membrane become more depolarized. Peak elevations of ΔF/F0 in 0 mM [Ca2+]e were ~5–10% of those evoked at the same membrane potential in 2 mM [Ca2+]e and exhibited an inverse U-shaped dependence on voltage. Both the rise and decay of ΔF/F0 transients in 0 mM [Ca2+]e were slower than those of ΔF/F0 transients evoked in 2 mM [Ca2+]e. Rises in ΔF/F0 evoked by high [K+]e in the absence of extracellular Ca2+ were blocked by thapsigargin, an inhibitor of endoplasmic reticulum Ca2+ ATPase, or the inositol 1,4,5-triphosphate (IP3) receptor antagonists 2-aminoethoxydiphenyl borate and xestospongin C, but not by extracellular Cd2+, the dihydropyridine antagonist nifedipine, or by ryanodine at concentrations that caused depletion of ryanodine-sensitive Ca2+ stores. These results support the notion that postganglionic sympathetic neurons possess the ability to release Ca2+ from IP3-sensitive internal stores in response to membrane depolarization, independent of Ca2+ influx.
Highlights
Calcium ions play an important role in regulating a variety of neuronal processes, including excitability, gene transcription, synaptic plasticity, growth cone behavior, synaptogenesis, and neurotransmitter release [1,2]
Whereas voltage-gated calcium channels and receptor-operated channels such as the NMDA receptors enable Ca2+ influx from the extracellular space, inositol 1,4,5-trisphosphate (IP3) receptors and ryanodine receptors distributed throughout the endoplasmic reticulum membrane are responsible for releasing Ca2+ from its internal stores [1]
To the best of our knowledge, the first evidence that postganglionic sympathetic neurons are capable of releasing Ca2+ from internal stores in response to prolonged depolarization in the absence of extracellular calcium
Summary
Calcium ions play an important role in regulating a variety of neuronal processes, including excitability, gene transcription, synaptic plasticity, growth cone behavior, synaptogenesis, and neurotransmitter release [1,2]. Neurons use both extracellular and intracellular sources of calcium. Voltage-induced, Ca2+ influx-independent, Ca2+ release form IP3-sensitive stores has been reported for insect dorsal unpaired median neurons [6]. Overall, these studies suggest the possibility that voltage-induced Ca2+ release from internal stores may be a more general phenomenon in neurons than previously thought
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