Epileptogenesis after traumatic brain injury in Plau-deficient mice
| Autor: | Tamuna Bolkvadze, Asla Pitkänen, Jukka Rantala, Noora Puhakka, Pedro Andrade |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Male
Traumatic brain injury Poison control Hippocampus Status epilepticus Epileptogenesis Mice 03 medical and health sciences Behavioral Neuroscience Epilepsy 0302 clinical medicine Neuroplasticity medicine Animals 030304 developmental biology Mice Knockout 0303 health sciences medicine.disease Urokinase-Type Plasminogen Activator nervous system diseases Mice Inbred C57BL Urokinase receptor Disease Models Animal Neurology Brain Injuries Disease Susceptibility Neurology (clinical) medicine.symptom Psychology Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Epilepsy & Behavior. 51:19-27 |
| ISSN: | 1525-5050 |
| Popis: | Several components of the urokinase-type plasminogen activator receptor (uPAR)-interactome, including uPAR and its ligand sushi-repeat protein 2, X-linked (SRPX2), are linked to susceptibility to epileptogenesis in animal models and/or humans. Recent evidence indicates that urokinase-type plasminogen activator (uPA), a uPAR ligand with focal proteinase activity in the extracellular matrix, contributes to recovery-enhancing brain plasticity after various epileptogenic insults such as traumatic brain injury (TBI) and status epilepticus. Here, we examined whether deficiency of the uPA-encoding gene Plau augments epileptogenesis after TBI. Traumatic brain injury was induced by controlled cortical impact in the somatosensory cortex of adult male wild-type and Plau-deficient mice. Development of epilepsy and seizure susceptibility were assessed with a 3-week continuous video-electroencephalography monitoring and a pentylenetetrazol test, respectively. Traumatic brain injury-induced cortical or hippocampal pathology did not differ between genotypes. The pentylenetetrazol test revealed increased seizure susceptibility after TBI (p |
| Databáze: | OpenAIRE |
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