Difference between revisions of "Burtscher J 2016 Abstract MitoFit Science Camp 2016"
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{{Abstract | {{Abstract | ||
|title=Oxidative phosphorylation in the healthy and | |title=Oxidative phosphorylation in the healthy and epileptic mouse brain. | ||
|authors=Burtscher J, Gnaiger E, Schwarzer C | |authors=Burtscher J, Gnaiger E, Schwarzer C | ||
|year=2016 | |year=2016 | ||
|event=MitoFit Science Camp 2016 Kuehtai AT | |event=MitoFit Science Camp 2016 Kuehtai AT | ||
|abstract=Mitochondrial dysfunction appears to be a common factor in neurodegenerative diseases. Strikingly, neurodegenerative diseases show regional specificity in vulnerability and follow distinct patterns of neuronal loss. A challenge is to understand, how mitochondrial failure in particular brain regions contributes to specific pathological conditions. | |abstract=Mitochondrial dysfunction appears to be a common factor in neurodegenerative diseases. Strikingly, neurodegenerative diseases show regional specificity in vulnerability and follow distinct patterns of neuronal loss. A challenge is to understand, how mitochondrial failure in particular brain regions contributes to specific pathological conditions [1]. | ||
High-resolution respirometry revealed significant differences of Complex I- and II- (CI and CII) linked oxidative phosphorylation (OXPHOS) capacity and coupling control between motor cortex, striatum, hippocampus and pons of naïve mice. CI-linked respiration was highest in motor cortex. In contrast, CII-linked capacity was especially important in the striatum. Apparent excess capacities of the electron transfer | High-resolution respirometry revealed significant differences of Complex I- and II- (CI and CII) linked oxidative phosphorylation (OXPHOS) capacity and coupling control between motor cortex, striatum, hippocampus and pons of naïve mice. CI-linked respiration was highest in motor cortex. In contrast, CII-linked capacity was especially important in the striatum. Apparent excess capacities of the electron transfer-pathway (ET-pathway) over OXPHOS also differed between regions. These differences may indicate risk factors for region-specific neuronal vulnerabilities. | ||
In the kainic acid (KA) model of temporal lobe epilepsy in mice, we observed markedly decreased absolute CI- and CII- linked oxygen consumption and also decreased | In the kainic acid (KA) model of temporal lobe epilepsy in mice, we observed markedly decreased absolute CI- and CII- linked oxygen consumption and also decreased ET-capacity in the injected dorsal hippocampus 2 days after KA. When normalized to ET-capacity, CII-linked respiration was significantly increased compared to controls. 3 weeks after KA-injection, tissue-mass specific CII-linked oxygen consumption reached control levels, but was elevated when normalized to ET-capacity. Tissue-mass specific CI-linked oxygen consumption and ET-capacity remained decreased. | ||
In summary, respirometric OXPHOS analysis allows detailed analysis of mitochondrial function from small amounts of specific | In summary, respirometric OXPHOS analysis allows detailed analysis of mitochondrial function from small amounts of specific brain regions (about 2 mg). It thus enables comparison of different brain tissues implicated in neurodegenerative diseases of the healthy mouse and disease models, while leaving enough material for further studies on the tissues.
| ||
|mipnetlab=AT Innsbruck Oroboros | |||
}} | |||
== Affiliations and Support== | |||
1-Dept Pharmacol, Med Univ Innsbruck; 2-D. Swarowski Research Lab, Dept Visceral, Transplant Thoracic Surgery, Med Univ Innsbruck; 3-Oroboros Instruments, Innsbruck; Austria. - johannes.burtscher@i-med.ac.at | |||
Supported by the Austrian Science Fund (FWF), project W1206-B05 | |||
# Burtscher J, Zangrandi L, Schwarzer C, Gnaiger E (2015) Differences in mitochondrial function in homogenated samples from healthy and epileptic specific brain tissues revealed by high-resolution respirometry. Mitochondrion 25:104-12. | |||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration | ||
|diseases=Neurodegenerative | |||
|organism=Mouse | |organism=Mouse | ||
|tissues=Nervous system | |tissues=Nervous system | ||
| | |preparations=Homogenate | ||
|couplingstates=OXPHOS, | |couplingstates=OXPHOS, ET | ||
| | |pathways=N, S | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|event=B2 | |||
|additional=MitoFit Science Camp 2016 | |additional=MitoFit Science Camp 2016 | ||
}} | }} | ||
Latest revision as of 18:45, 10 January 2022
Oxidative phosphorylation in the healthy and epileptic mouse brain. |
Link:
Burtscher J, Gnaiger E, Schwarzer C (2016)
Event: MitoFit Science Camp 2016 Kuehtai AT
Mitochondrial dysfunction appears to be a common factor in neurodegenerative diseases. Strikingly, neurodegenerative diseases show regional specificity in vulnerability and follow distinct patterns of neuronal loss. A challenge is to understand, how mitochondrial failure in particular brain regions contributes to specific pathological conditions [1].
High-resolution respirometry revealed significant differences of Complex I- and II- (CI and CII) linked oxidative phosphorylation (OXPHOS) capacity and coupling control between motor cortex, striatum, hippocampus and pons of naïve mice. CI-linked respiration was highest in motor cortex. In contrast, CII-linked capacity was especially important in the striatum. Apparent excess capacities of the electron transfer-pathway (ET-pathway) over OXPHOS also differed between regions. These differences may indicate risk factors for region-specific neuronal vulnerabilities.
In the kainic acid (KA) model of temporal lobe epilepsy in mice, we observed markedly decreased absolute CI- and CII- linked oxygen consumption and also decreased ET-capacity in the injected dorsal hippocampus 2 days after KA. When normalized to ET-capacity, CII-linked respiration was significantly increased compared to controls. 3 weeks after KA-injection, tissue-mass specific CII-linked oxygen consumption reached control levels, but was elevated when normalized to ET-capacity. Tissue-mass specific CI-linked oxygen consumption and ET-capacity remained decreased.
In summary, respirometric OXPHOS analysis allows detailed analysis of mitochondrial function from small amounts of specific brain regions (about 2 mg). It thus enables comparison of different brain tissues implicated in neurodegenerative diseases of the healthy mouse and disease models, while leaving enough material for further studies on the tissues.
• O2k-Network Lab: AT Innsbruck Oroboros
Affiliations and Support
1-Dept Pharmacol, Med Univ Innsbruck; 2-D. Swarowski Research Lab, Dept Visceral, Transplant Thoracic Surgery, Med Univ Innsbruck; 3-Oroboros Instruments, Innsbruck; Austria. - johannes.burtscher@i-med.ac.at
Supported by the Austrian Science Fund (FWF), project W1206-B05
- Burtscher J, Zangrandi L, Schwarzer C, Gnaiger E (2015) Differences in mitochondrial function in homogenated samples from healthy and epileptic specific brain tissues revealed by high-resolution respirometry. Mitochondrion 25:104-12.
Labels: MiParea: Respiration
Pathology: Neurodegenerative
Organism: Mouse Tissue;cell: Nervous system Preparation: Homogenate
Coupling state: OXPHOS, ET
Pathway: N, S
HRR: Oxygraph-2k
Event: B2
MitoFit Science Camp 2016