| dc.creator |
Núñez, Lucía |
|
| dc.creator |
Senovilla, Laura |
|
| dc.creator |
Sanz-Blasco, Sara |
|
| dc.creator |
Chamero, Pablo |
|
| dc.creator |
Alonso, María Teresa |
|
| dc.creator |
Villalobos, Carlos |
|
| dc.creator |
García-Sancho, Javier |
|
| dc.date |
2008-06-20T07:23:35Z |
|
| dc.date |
2008-06-20T07:23:35Z |
|
| dc.date |
2007-04-15 |
|
| dc.date.accessioned |
2017-01-31T01:44:25Z |
|
| dc.date.available |
2017-01-31T01:44:25Z |
|
| dc.identifier |
Journal of Physiology 580(2): 385–395 (2007) |
|
| dc.identifier |
0022-3751 |
|
| dc.identifier |
http://hdl.handle.net/10261/5198 |
|
| dc.identifier |
10.1113/jphysiol.2006.126524 |
|
| dc.identifier.uri |
http://dspace.mediu.edu.my:8181/xmlui/handle/10261/5198 |
|
| dc.description |
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. |
|
| dc.description |
This work was supported by grants from Junta de Castilla y León (VA071/02; VA022A05), Ministerio de Educación y Ciencia (MEC; BFU2004-02764), Fondo de Investigaciones Sanitarias FIS 04/1510 and Ministerio de Sanidad, Instituto de Salud Carlos III, Red de Terapia Celular. L.N. is fellow of the Ramón y Cajal Program (MEC and FEDER-FSE). L.S. is the recipient of a predoctoral fellowship from MEC. Pablo Chamero held a predoctoral fellowship from the Basque Government. |
|
| dc.description |
Peer reviewed |
|
| dc.format |
22195 bytes |
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| dc.format |
application/pdf |
|
| dc.language |
eng |
|
| dc.publisher |
Wiley-Blackwell |
|
| dc.rights |
closedAccess |
|
| dc.title |
Bioluminescence imaging of mitochondrial Ca2+ dynamics in soma and neurites of individual adult mouse sympathetic neurons |
|
| dc.type |
Artículo |
|