TY - JOUR
T1 - Sensory neurons respond to hypoxia with NO production associated with mitochondria
AU - Henrich, Michael
AU - Hoffmann, Karin
AU - König, Peter
AU - Gruß, Marco
AU - Fischbach, Tamara
AU - Gödecke, Axel
AU - Hempelmann, Gunter
AU - Kummer, Wolfgang
N1 - Funding Information:
We thank Andreas Scholz, Giessen, for providing samples of neuronal cytoplasm collected during intracellular recording experiments, Silke Wiegand, Martin Bodenbenner, and Gerhard Kripp for skillful technical assistance and Karola Michael for figure layout. This study was supported by the DFG (SFB 547, Project C1; GK 534).
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2002
Y1 - 2002
N2 - Oxygen is pivotal for mammalian cell function, and recent studies suggest an 3involvement of NO in cellular adaptation to low oxygen supply. Here, we report that endothelial NO-synthase is ubiquitously expressed in rat and mice sensory neurons, and is targeted to juxtamitochondrial compartments of the ER. There it is activated in response to hypoxia while generation of reactive oxygen species remains unaltered. Developing a technique for ultrastructural localization of an NO-sensitive indicator allowed to identify the inner mitochondrial membrane as the target of NO under hypoxia. The demonstrated hypoxic stimulation of endothelial NOS in sensory neurons shall contribute to resistance against hypoxia, since NO promotes cellular survival by interfering with mitochondrial function.
AB - Oxygen is pivotal for mammalian cell function, and recent studies suggest an 3involvement of NO in cellular adaptation to low oxygen supply. Here, we report that endothelial NO-synthase is ubiquitously expressed in rat and mice sensory neurons, and is targeted to juxtamitochondrial compartments of the ER. There it is activated in response to hypoxia while generation of reactive oxygen species remains unaltered. Developing a technique for ultrastructural localization of an NO-sensitive indicator allowed to identify the inner mitochondrial membrane as the target of NO under hypoxia. The demonstrated hypoxic stimulation of endothelial NOS in sensory neurons shall contribute to resistance against hypoxia, since NO promotes cellular survival by interfering with mitochondrial function.
UR - http://www.scopus.com/inward/record.url?scp=0036318683&partnerID=8YFLogxK
U2 - 10.1006/mcne.2002.1111
DO - 10.1006/mcne.2002.1111
M3 - Journal articles
C2 - 12093162
AN - SCOPUS:0036318683
SN - 1044-7431
VL - 20
SP - 307
EP - 322
JO - Molecular and Cellular Neuroscience
JF - Molecular and Cellular Neuroscience
IS - 2
ER -
