Burtscher J 2012 Abstract Bioblast

From Bioblast
Burtscher J, Eigentler A, Gnaiger E, Schwarzer C (2012) Mitochondrial function in the mouse hippocampus. Mitochondr Physiol Network 17.12.

Link: MiPNet17.12 Bioblast 2012 - Open Access

Burtscher J, Eigentler A, Gnaiger E, Schwarzer C (2012)

Event: Bioblast 2012

Johannes Burtscher

Epilepsy is one of the most common neurological diseases featuring a prevalence of 1-2%. A high percentage of patients is refractory to antiepileptic medication, especially in mesial temporal lobe epilepsy (mTLE). Epilepsy is characterized by seizures, in which a lot of glutamate is released leading to excitotoxicity and neuronal loss. Seizure related alterations in neurons are often associated with damaged mitochondria and with impaired functions of distinct complexes of the electron transport chain in human patients and animal models. However, mitochondrial alterations during the development of epilepsy (epileptogenesis) are not well characterized and it is not yet known, whether mitochondrial alterations are cause or consequence of epileptogenesis. Answers to these questions are important to learn more about the neurochemical processes underlying epileptogenesis and to assess implications on the development of antiepilept(ogen)ic medication. Therefore, we are in the process of developing protocols to analyze different mitochondrial parameters using the Oxygraph-2K (Oroboros Instruments, Innsbruck) in hippocampal tissue - which is strongly affected in mTLE - of mice. We apply the kainic acid model of TLE in mice. Injection of kainic acid into the hippocampal CA1 region results in Status epilepticus, a subsequent silent phase and ultimately recurrent seizures. We want to study the activities of electron transport chain (ETC) complexes I, II and IV across different time points of these phases of epileptogenesis.

  1. Kudin AP, Kudina TA, Seyfried J, Vielhaber S, Beck H, Elger CE, Kunz WS (2002) Seizure-dependent modulation of mitochondrial oxidative phosphorylation in rat hippocampus. Eur J Neurosci 15: 1105-1114.
  2. McNamara JO (1999) Emerging insights into the genesis of epilepsy. Nature 399: A15-22.
  3. Milatovic D, Zivin M, Gupta RC, Dettbarn WD (2001) Alterations in cytochrome c oxidase activity and energy metabolites in response to kainic acid-induced status epilepticus. Brain Res 912: 67-78.

β€’ Keywords: Epilepsy, Kainic Acid

β€’ O2k-Network Lab: AT Innsbruck Oroboros


Stress:Mitochondrial disease  Organism: Mouse  Tissue;cell: Nervous system  Preparation: Homogenate  Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex IV;cytochrome c oxidase 

Pathway: N, S, CIV  HRR: Oxygraph-2k 

Affiliations and author contributions

Burtscher Johannes (1), Eigentler Andrea (2), Gnaiger Erich (2, 3), Christoph Schwarzer (1)

(1) Institute of Pharmacology; Innsbruck, Austria; Email: johannes.burtscher@student.uibk.ac.at

(2) Medical University of Innsbruck, Department of Visceral, Transplant and Thoracic Surgery, D. Swarovski Research Laboratory, Innsbruck, Austria

(3) Oroboros Instruments Corp, High-Resolution Respirometry, Innsbruck, Austria


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