Burtscher J 2012 Abstract Bioblast

Burtscher J (2012) Mitochondrial involvement in epileptogenesis. Mitochondr Physiol Network 17.12.

Link: MiPNet17.12 Bioblast 2012 - Open Access

Burtscher J (2012)

Event: Bioblast 2012

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.

• Keywords: Epilepsy, Kainic Acid

• O2k-Network Lab: AT Innsbruck OROBOROS

Labels:

Stress:Mitochondrial Disease; Degenerative Disease and Defect"Mitochondrial Disease; Degenerative Disease and Defect" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.  Organism: Mouse  Tissue;cell: Neurons; Brain"Neurons; Brain" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.  Preparation: Homogenate  Enzyme: Complex I, Complex II; Succinate Dehydrogenase"Complex II; Succinate Dehydrogenase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property., Complex IV; Cytochrome c Oxidase"Complex IV; Cytochrome c Oxidase" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property. 

HRR: Oxygraph-2k 

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