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This Article Full Text Full Text (PDF) All Versions of this Article: 580/2/385    most recent jphysiol.2006.126524v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Núñez, L. Articles by García-Sancho, J. Search for Related Content PubMed PubMed Citation Articles by Núñez, L. Articles by García-Sancho, J. Related Collections Neuroscience

¹ Instituto de Biología y Genética Molecular (IBGM), Universidad de Valladolid and Consejo Superior de Investigaciones Científicas (CSIC), c/Sanz y Forés s/n, 47003 Valladolid, Spain

Changes in the cytosolic Ca²⁺ concentration ([Ca²⁺]_c) are essential for triggering neurotransmitter release from presynaptic nerve terminals. Calcium-induced Ca²⁺ release (CICR) from the endoplasmic reticulum (ER) may amplify the [Ca²⁺]_c signals and facilitate neurotransmitter release in sympathetic neurons. In adrenal chromaffin cells, functional triads are formed by voltage-operated Ca²⁺ channels (VOCCs), CICR sites and mitochondria. In fact, mitochondria take up most of the Ca²⁺ load entering the cells and are essential for shaping [Ca²⁺]_c signals and exocytosis. Here we have investigated the existence of such functional triads in sympathetic neurons. The mitochondrial Ca²⁺ concentration ([Ca²⁺]_m) in soma and neurites of individual mouse superior cervical ganglion (SCG) neurons was monitored by bioluminescence imaging of targeted aequorins. In soma, Ca²⁺ entry through VOCCs evoked rapid, near millimolar [Ca²⁺]_m increases in a subpopulation of mitochondria containing about 40% of the aequorin. Caffeine evoked a similar [Ca²⁺]_m increase in a mitochondrial pool containing about 30% of the aequorin and overlapping with the VOCC-sensitive pool. These observations suggest the existence of functional triads similar to the ones described in chromaffin cells. In neurites, mitochondria were able to buffer [Ca²⁺]_c increases resulting from activation of VOCCs but not those mediated by caffeine-induced Ca²⁺ release from the ER. The weaker Ca²⁺ buffering by mitochondria in neurites could contribute to facilitate Ca²⁺-induced exocytosis at the presynaptic sites.

(Received 13 December 2006; accepted after revision 18 January 2007; first published online 18 January 2007)
Corresponding author L. Núñez: Instituto de Biología y Genética Molecular (IBGM), Universidad de Valladolid and CSIC, c/ Sanz y Forés s/n, 47003 Valladolid, Spain.  Email: nunezl{at}ibgm.uva.es