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. 2009 Feb 4;64A(1):34–44. doi: 10.1093/gerona/gln053

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© 2009 The Author(s).

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 1. — Model of the superior cervical ganglion (SCG) cell and illustrated protocol used in this study. In SCG cells, calcium transients are modulated by numerous mechanisms including influx via voltage-gated calcium channels, calcium-induced calcium release (CICR), and transport of calcium by smooth endoplasmic reticulum Ca²⁺-ATPases, which both buffers [Ca²⁺]_i transients and refills smooth endoplasmic reticulum (SER) calcium stores to maintain regenerative CICR. CICR is mediated via ryanodine receptors, which can be inhibited or activated using ryanodine or caffeine, respectively (see Methods). In this study, electrical field stimulation was used to evoke calcium influx, which activates CICR from SER calcium stores. Influx and CICR contribute to the magnitude of the measured variable, [Ca²⁺]_i as detected by fura-2 fluorescence.