Metabolic Changes in Early Poststatus Epilepticus Measured by MR Spectroscopy in Rats

Autor: Nihal C. de Lanerolle, Patrice Pearce, Yijen L. Wu, T. Kevin Hitchens, Amedeo Rapuano, Jullie W. Pan
Rok vydání: 2015
Předmět:
Male
In vivo magnetic resonance spectroscopy
medicine.medical_specialty
Kainic acid
Pathology
Magnetic Resonance Spectroscopy
Glutamine
glutamate
Nerve Tissue Proteins
Status epilepticus
Temporal lobe
Rats
Sprague-Dawley
03 medical and health sciences
chemistry.chemical_compound
Epilepsy
Status Epilepticus
0302 clinical medicine
Internal medicine
energy metabolism
medicine
Animals
030304 developmental biology
Brain Chemistry
Aspartic Acid
0303 health sciences
neuronal–glial interactions
Kainic Acid
business.industry
T-cell receptor
Glutamate receptor
Antigens
Nuclear
Macrophage Activation
Creatine
medicine.disease
Rats
Endocrinology
Epilepsy
Temporal Lobe
Neurology
chemistry
epilepsy
Original Article
Neurology (clinical)
medicine.symptom
Cardiology and Cardiovascular Medicine
business
Neuroglia
Inositol
030217 neurology & neurosurgery
Zdroj: Journal of Cerebral Blood Flow & Metabolism
ISSN: 1559-7016
0271-678X
Popis: There is little experimental in vivo data on how differences in seizure duration in experimental status epilepticus influence metabolic injury. This is of interest given that in humans, status duration is a factor that influences the probability of subsequent development of epilepsy. This question is studied using 7-T magnetic resonance (MR) spectroscopy, T2 relaxometry in the incremented kainate rodent model of temporal lobe epilepsy, using two durations of status epilepticus, 1.5 and 3 hours. Histologic evaluation was performed in a subset of animals. Three days after status, single-voxel (8 mm3) point resolved spectroscopy (PRESS) MR spectroscopic measurements were acquired at 7 T to assess the cerebral metabolites measured as a ratio to total creatine (tCr). The status injury resulted in decreased N-acetylaspartate NAA/tCr, increased myo-inositol/tCr and glutamine/tCr, increased T2, and significant declines in NeuN-stained neuronal counts in both status groups. Regressions were identified in the status groups that provide evidence for neuronal injury and astrocytic reaction after status in both the short and long status duration groups. The long status group displays changes in glutathione/tCr that are not identified in the short status group, this difference possibly representing a maturation of injury and antioxidant response that occurs in synchrony with glutamatergic injury and glial activation.
Databáze: OpenAIRE
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