Ca2+-induced Ca2+ release mediates a slow post-spike hyperpolarization in rabbit vagal afferent neurons.

The relation between Ca2+-induced Ca2+ release (CICR) elicited by action potentials (APs) and a Ca2+-dependent slow post-spike hyperpolarization (AHPslow) in acutely dissociated adult rabbit nodose neurons was studied using microfluorimetric calcium measurements in conjunction with standard intracellular current- and voltage-clamp recording techniques. The magnitude of the AP-induced transient increase in [Ca2+]i (DeltaCat) was used to monitor CICR. There was a close correlation between the magnitude of the DeltaCat and the AHPslow current over the range of 1-16 APs (r = 0.985). Functional CICR blockers, ryanodine (10 muM), thapsigargin (100 nM), 2,5-di(t-butyl)hydroquinone (10 muM) or cyclopiazonic acid (10 muM), selectively reduced the peak amplitude of the AHPslow >/=91%. In five neurons, simultaneous recordings of the DeltaCat and the AHPslow revealed that both responses were blocked in parallel. These findings indicate that CICR is necessary for the generation of the AHPslow in rabbit nodose neurons. The DeltaCat rises and decays significantly faster than the AHPslow. This temporal disparity suggests that activation of the AHPslow by Ca2+ may require additional signal transduction steps.