Ca(2+)‐induced Ca2+ release and its activation in response to a single action potential in rabbit otic ganglion cells.

Dysregulated IP3Signaling in Cortical Neurons of Knock-In Mice Expressing an Alzheimer's-Linked Mutation inPresenilin1Results in Exaggerated Ca2+Signals and Altered Membrane Excitability

“…The PS1 mutation results, therefore, not only in an exaggeration of IP 3 -evoked Ca 2ϩ signals in responding neurons but appears to shift weak and nonresponders to strong responders. The heterogeneity of IP 3 -evoked Ca 2ϩ responses likely reflects the recent Ca 2ϩ filling or release history of the ER (Yoshizaki et al, 1995;Garaschuk et al, 1997), and we had demonstrated that nonresponding neurons could sometimes be rescued by allowing the ER to fill via Ca 2ϩ entry during action potentials (Stutzmann et al, 2003). Thus, ER Ca 2ϩ stores in most neurons from PS1 KI mice are likely overfilled, with possible subsequent consequences for neuronal signaling, metabolism, and neuropathology.…”

Ca2+ images and K+ current during depolarization in smooth muscle cells of the guinea‐pig vas deferens and urinary bladder

“…The large contribution of IK,Ca activated by superficial CICR to the negative feedback of membrane excitability andÏor the regulation of action potential shape is characteristic of smooth muscle cells (Imaizumi et al 1996a). Although the regulation of membrane excitability by CICR from SRÏER via activation of IK,Ca has been reported in some neurons (Kuba, 1994;Yoshizaki et al 1995;Cohen, Moore, Bangalore, Jafri, Weinreich & Kao, 1997), high time-resolution spatial analyses of Ca¥ release from the SRÏER have not yet been done.…”

Ca2+ release from internal stores: role in generating depolarizing after‐potentials in rat supraoptic neurones.

“…In comparison with guinea-pig vagal and rat otic ganglion neurones, SON neurones appear to rely less on Ca2+ release to generate DAPs, as application of ryanodine at the same concentration level as used to eliminate slow AHPs (Sah & MIcLachlan, 1991;Yoshizaki et al 1995) . i , , .…”

“…An increasing body of evidence indicates that CICR is involved in modulation of cell excitability, neurotransmitter release from nerve terminals, expression of immediate-early genes, long-term potentiation and Ca2+ oscillations (Henzi & MacDermott, 1992). In particular, blockade of CICR in CNS neurones has been shown to suppress slow after-hyperpolarizations (AHPs), Ca2 -dependent potentials with time courses overlapping those of DAPs (Sah & McLachlan, 1991;Yoshizaki et al 1995). The features of both Ca2 -dependent DAPs and Ca + release from internal stores, therefore, led us to examine whether DAP generation in SON neurones involves CICR.…”