Advancing age alters intracellular calcium buffering in rat adrenergic nerves

Mitochondria and aging: a role for the permeability transition?

“…It has been reported (Morgan & Jacob, 1994) ] following depolarization-induced Ca 2+ transients is frequently impaired (e.g. Villalba et al, 1995;Buchholz et al, 1996). As argued by Buchholz et al (1996), this will place greater reliance on mitochondria in shaping the Ca 2+ transients.…”

“…Villalba et al, 1995;Buchholz et al, 1996). As argued by Buchholz et al (1996), this will place greater reliance on mitochondria in shaping the Ca 2+ transients. In broad support, when the uncoupler DNP was used to limit mitochondrial Ca 2+ uptake, the transient amplitude was increased in senescent cells (superior cervical ganglion), but not in adults.…”

Calcium Regulation in Neuronal Function with Advancing Age: Limits of Homeostasis

“…To follow up, SCG neurons were exposed to DNP to block mitochondrial calcium uptake, and [Ca 2+ ]i transients were measured. The peak and rate of rise of high K + -evoked [Ca 2+ ]i transients were both increased in neurons from old animals with no significant effect in young neurons (Buchholz et al, 1996). In another study we blocked PMCA, SERCA, and Na + /Ca 2+ exchangers from participating in calcium buffering in SCG neurons.…”

“…In contrast to this view, however, mitochondrial calcium uptake has been shown to produce a clear "mitochondrial set point" or shoulder in the shape of depolarization evoked [Ca 2+ ]i, transients in central and peripheral sensory neurons (Thayer et al, 1994;Murchison et al, 2004). Furthermore, proton motive force disruptors such as dinitrophenol (DNP) and carbonyl cyanide m-chlorophenyl hydrazone (CCCP) demonstrate the role of mitochondria in buffering normal [Ca 2+ ]i transients (Thayer & Miller, 1990;Miller, 1991;Werth and Thayer, 1994;Buchholz et al, 1996;Murchinson & Griffith, 1999;Colegrove et al, 2000, Murchison et al, 2004. Thus, it is clear that mitochondria play a role in shaping stimulation-evoked [Ca 2+ ]i transients in central and peripheral sensory and sympathetic neurons under normal [Ca 2+ ]i concentrations in the mid to high nanomolar ranges.…”

“…Buffering systems include calcium-buffering proteins, energy dependent SER Ca 2+ ATPases (SERCA), plasmalemmal Ca 2+ -ATPases (PMCA), mitochondrial Ca 2+ /H + symporters and Na + /Ca 2+ -exchangers. All of these calcium buffering systems act to modulate the shape and magnitude of stimulus-evoked [Ca 2+ ]i transients and contribute to restoration of [Ca 2+ ]i levels (Werth & Thayer, 1994;Buchholz et al, 1996;Werthet al, 1996;Usachev & Thayer, 1999a;Pottorf et al ., a,c , 2002Wuytack et al, 2002). Furthermore, the SERCA function and the CICR process are interdependent, as SERCA pumps not only buffer [Ca 2+ ]i transients but also refill SER calcium stores.…”