CA2-INDUCED CA2+ RELEASE MEDIATES A SLOW POST-SPIKE HYPERPOLARIZATIONIN RABBIT VAGAL AFFERENT NEURONS()

The relation between Ca2+-induced Ca2+ release (CICR) elicited by acti on potentials (APs) and a Ca2+-dependent slow post-spike hyperpolariza tion (AHP(slow)) in acutely dissociated adult rabbit nodose neurons wa s studied using microfluorimetric calcium measurements in conjunction with standard intracellular current- and voltage-clamp recording techn iques. The magnitude of the AP-induced transient increase in [Ca2+](i) (Delta Ca-t) was used to monitor CICR. There was a close correlation between the magnitude of the Delta Ca-t and the AHP(slow) current over the range of 1-16 APs (r = 0.985). Functional CICR blockers, ryanodin e (10 mu M), thapsigargin (100 nM), 2,5-di(t-butyl)hydroquinone (10 mu M) or cyclopiazonic acid (100 nM), selectively reduced the peak ampli tude of the AHP(slow) greater than or equal to 91%. In five neurons, s imultaneous recordings of the Delta Ca-t and the AHP(slow) revealed th at both responses were blocked in parallel. These findings indicate th at CICR is necessary for the generation of the AHP(slow) in rabbit nod ose neurons. The Delta Ca-t rises and decays significantly faster than the AHP(slow). This temporal disparity suggests that activation of th e AHP(slow) by Ca2+ may require additional signal transduction steps.