Temperature and nitric oxide control spontaneous calcium transients in astrocytes

Modeling the spontaneousCa2+oscillations in astrocytes: Inconsistencies and usefulness

“…These authors tried to find an explanation to the contrasting high and low frequency of SCOs observed with ex vivo and in vivo experiments, respectively. Note that the percentage of active astrocytes in WT mice reported by Riera et al (2011) (61.66%, 10 min, 15%, absolute value) was equivalent to those reported by Schipke et al (2008) at the corresponding 466 J. RIERA ET AL.…”

“…Actually, Schipke et al (2008) found that temperature constitutes a major determinant of SCOs in astrocytes. These authors tried to find an explanation to the contrasting high and low frequency of SCOs observed with ex vivo and in vivo experiments, respectively.…”

Fundamental properties of Ca2+ signals

“…For example, stochastic models reproduce the sensitive dependence of the average ISI on the diffusional properties of the cytosol, while deterministic models predict independence of the average ISI from diffusion coefficients and buffer concentrations [26,36]. Similar considerations apply to other correlations [16,26,37,38]. Stochastic models reconcile dissociation constants of the Ca 2+ regulatory binding sites on the IP 3 R measured in vitro with the dynamic behavior and local concentrations in vivo [17], and they offer straightforward explanations for the large measured cell-to-cell variability of the average ISI [36,39].…”

Cumulated Ca2+ spike duration underlies Ca2+ oscillation frequency-regulated NFκB transcriptional activity

“…This novel and unique understanding is of importance because [Ca 2+ ] i SD can be fundamentally modulated by lots of physiological and pathophysiological circumstances: high agonist concentration increases [Ca 2+ ] i SD in epidermal growth factor-stimulated endothelial cells (Moccia et al, 2002) and carbachol-stimulated avian nasal gland cells (Shuttleworth and Thompson, 1996); agonist species modulates [Ca 2+ ] i SD in hepatocytes (Cobbold et al, 1991); high extracellular Ca 2+ concentration prolongs [Ca 2+ ] i SD in human chorionic gonadotropin-induced aged oocyte (Igarashi et al, 1997) and cholecystokinin-stimulated pancreatic acinar cell (Zhao et al, 1990); increasing extracellular pH increases [Ca 2+ ] i SD in cholecystokinin-stimulated pancreatic acinar cell (Zhao et al, 1990) and high-K + -stimulated dorsal root ganglion neurons (Jackson and Thayer, 2006); endoplasmic reticulum Ca 2+ -ATPase inhibition increases [Ca 2+ ] i SD in pancreatic acinar cells (Petersen et al, 1993); PKC activators or a constitutively active PKC isoform b1 increases [Ca 2+ ] i SD in HEK-293 cells (Young et al, 2002); and the mitochondrial electron transport uncoupler FCCP reduces, whereas mitochondrial ATP synthase inhibitor oligomycin B increases [Ca 2+ ] i SD, in high-K + -stimulated dorsal root ganglion neurons (Jackson and Thayer, 2006); lowering temperature prolongs [Ca 2+ ] i SD in neocortical pyramidal neurons (Lee et al, 2005), cortical astrocytes (Schipke et al, 2008) and HEK-293 cells (Szekely et al, 2009 …”

“…Here, we hypothesized that [Ca 2+ ] i oscillation frequency regulates transcription through a mechanism associated with the cumulated time duration of [Ca 2+ ] i elevations. The cumulated time duration of [Ca 2+ ] i elevations is controlled by frequency, but another determinant is [Ca 2+ ] i spike duration (SD) or [Ca 2+ ] i spike width, which is profoundly modulated by a variety of extracellular and intracellular conditions or physiological and pathophysiological circumstances, such as agonist species and their concentration (Cobbold et al, 1991;Moccia et al, 2003;Morgan and Jacob, 1998;Shuttleworth and Thompson, 1996), extracellular Ca 2+ concentration (Igarashi et al, 1997;Zhao et al, 1990), extracellular pH (Jackson and Thayer, 2006;Zhao et al, 1990), the endoplasmic reticulum Ca 2+ -ATPase (Morgan and Jacob, 1998;Petersen et al, 1993), protein kinase C (PKC) (Young et al, 2002), mitochondria (Jackson and Thayer, 2006) and even temperature (Lee et al, 2005;Schipke et al, 2008;Szekely et al, 2009 ] i oscillation models alone, with a 'Ca 2+ clamp' method (Dolmetsch et al, 1998;Tomida et al, 2003;Zhu et al, 2008), and using [Ca 2+ ] i oscillation models in the concomitant presence of agonist stimulation (Zhu et al, 2008) or repetitive pulses of agonist exposure (Bootman et al, 1994;Morgan and Jacob, 1998), are employed. A human bronchial epithelial cell line, 16HBE, is adapted in these experiments so that it stably expresses histamine receptor, and the responsiveness to the Ca 2+ -dependent pathways of NFkB, Oct and NFAT activity to agonists (Profita et al, 2008;Sidhaye et al, 2008;Weber et al, 2001), including his...…”