Alterations in calcium-mediated signal transduction after traumatic injury of cortical neurons
| Autor: | Beverly A. Rzigalinski, Earl F. Ellis, Karen A. Willoughby, S. F. Moore, John T. Weber |
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| Rok vydání: | 2000 |
| Předmět: |
medicine.medical_specialty
N-Methylaspartate Physiology Traumatic brain injury chemistry.chemical_element Glutamic Acid Calcium Biology Calcium in biology Rats Sprague-Dawley Internal medicine medicine Excitatory Amino Acid Agonists Animals Cycloleucine Calcium Signaling Enzyme Inhibitors Molecular Biology Cells Cultured Calcium signaling Calcium metabolism Cerebral Cortex Neurons Glutamate receptor Cell Biology medicine.disease Rats Endocrinology Traumatic injury Neuroprotective Agents chemistry Anesthesia Brain Injuries NMDA receptor Thapsigargin Neuroglia |
| Zdroj: | Cell calcium. 26(6) |
| ISSN: | 0143-4160 |
| Popis: | Calcium influx and elevation of intracellular free calcium ([Ca2+]i), with subsequent activation of degradative enzymes, is hypothesized to cause cell injury and death after traumatic brain injury. We examined the effects of mild-to-severe stretch-induced traumatic injury on [Ca2+]i dynamics in cortical neurons cultured on silastic membranes. [Ca2+]i was rapidly elevated after injury, however, the increase was transient with neuronal [Ca2+]i returning to basal levels by 3 h after injury, except in the most severely injured cells. Despite a return of [Ca2+]i to basal levels, there were persistent alterations in calcium-mediated signal transduction through 24 h after injury. [Ca2+]i elevation in response to glutamate or NMDA was enhanced after injury. We also found novel alterations in intracellular calcium store-mediated signaling. Neuronal calcium stores failed to respond to a stimulus 15 min after injury and exhibited potentiated responses to stimuli at 3 and 24 h post-injury. Thus, changes in calcium-mediated cellular signaling may contribute to the pathology that is observed after traumatic brain injury. |
| Databáze: | OpenAIRE |
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