Burtscher J 2012 Abstract Bioblast

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

Link: MiPNet17.12 Bioblast 2012 - Open Access

Burtscher J (2012)

Event: [[Was submitted to event::Bioblast 2012]]

[[has abstract::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.]]

β€’ Keywords: Epilepsy, Kainic Acid

β€’ O2k-Network Lab: AT Innsbruck OROBOROS


Labels:

Stress:Mitochondrial Disease; Degenerative Disease and Defect  Organism: Mouse  Tissue;cell: Neurons; Brain  Preparation: Homogenate  Enzyme: Complex I, Complex II; Succinate Dehydrogenase, Complex IV; Cytochrome c Oxidase 


HRR: Oxygraph-2k 




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