Difference between revisions of "Morato 2016 Abstract IOC116"
(Created page with "{{Abstract |info=Mitochondr Physiol Network 21.11 |year=2016 |event=IOC116 }} {{Labeling}} == Affiliations ==") |
|||
| Line 1: | Line 1: | ||
{{Abstract | {{Abstract | ||
|title=Impaired mitochondrial function mediates early life stress-induced depression. | |||
|info=Mitochondr Physiol Network 21.11 | |info=Mitochondr Physiol Network 21.11 | ||
|authors=Morato L, Guillot de Suduiraut MI, Grosse J, Zanoletti O, Riccio O, Fournier C, Sandi C | |||
|year=2016 | |year=2016 | ||
|event=IOC116 | |event=IOC116 | ||
|abstract=Early-life exposure to stressful experiences has been described as a predisposing factor to develop psychopathologies including anxiety and depression. In our lab, we outlined a paradigm of unpredictable stress in C57BL/6 mice that aims to model exposure to fearful experiences during childhood and puberty. We observed that stressed animals present increased anxiety, depression-like behaviors and decreased sociability. Aiming at understanding the neuronal mechanisms whereby early life stress can induce these behavioral alterations, we performed a gene expression analysis in the nucleus accumbens, a critical brain region for the stress response. Remarkably, we observed that the nucleus accumbens of stressed animals exhibits a reduced expression of master-regulators of mitochondrial function such as SIRT1 and PGC-1a, concomitant with a reduction in mitochondrial respiration measured by high-resolution respirometry. These findings might pave the way for the use of mitochondrial boosters to treat stress-related disorders such as depression. | |||
|mipnetlab=CH Lausanne Sandi C | |||
}} | |||
{{Labeling | |||
|area=Respiration, nDNA;cell genetics, Exercise physiology;nutrition;life style, mt-Medicine, mt-Awareness | |||
|organism=Mouse | |||
|injuries=Mitochondrial disease | |||
|diseases=Other | |||
|instruments=Oxygraph-2k | |||
}} | }} | ||
== Affiliations == | == Affiliations == | ||
1-Lab Behavioral Genetics, Brain Mind Inst, École Polytechnique Fédérale de Lausanne, Switzerland. - laia.moratofornaguera@epfl.ch | |||
Revision as of 14:45, 24 October 2016
| Impaired mitochondrial function mediates early life stress-induced depression. |
Link: Mitochondr Physiol Network 21.11
Morato L, Guillot de Suduiraut MI, Grosse J, Zanoletti O, Riccio O, Fournier C, Sandi C (2016)
Event: IOC116
Early-life exposure to stressful experiences has been described as a predisposing factor to develop psychopathologies including anxiety and depression. In our lab, we outlined a paradigm of unpredictable stress in C57BL/6 mice that aims to model exposure to fearful experiences during childhood and puberty. We observed that stressed animals present increased anxiety, depression-like behaviors and decreased sociability. Aiming at understanding the neuronal mechanisms whereby early life stress can induce these behavioral alterations, we performed a gene expression analysis in the nucleus accumbens, a critical brain region for the stress response. Remarkably, we observed that the nucleus accumbens of stressed animals exhibits a reduced expression of master-regulators of mitochondrial function such as SIRT1 and PGC-1a, concomitant with a reduction in mitochondrial respiration measured by high-resolution respirometry. These findings might pave the way for the use of mitochondrial boosters to treat stress-related disorders such as depression.
• O2k-Network Lab: CH Lausanne Sandi C
Labels: MiParea: Respiration, nDNA;cell genetics, Exercise physiology;nutrition;life style, mt-Medicine, mt-Awareness Pathology: Other Stress:Mitochondrial disease Organism: Mouse
HRR: Oxygraph-2k
Affiliations
1-Lab Behavioral Genetics, Brain Mind Inst, École Polytechnique Fédérale de Lausanne, Switzerland. - laia.moratofornaguera@epfl.ch
