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- Title
Traumatic brain injury causes a long-lasting calcium (Ca<sup>2+</sup>)-plateau of elevated intracellular Ca levels and altered Ca<sup>2+</sup> homeostatic mechanisms in hippocampal neurons surviving brain injury.
- Authors
Sun, David A.; Deshpande, Laxmikant S.; Sombati, Sompong; Baranova, Anya; Wilson, Margaret S.; Hamm, Robert J.; DeLorenzo, Robert J.
- Abstract
Traumatic brain injury (TBI) survivors often suffer chronically from significant morbidity associated with cognitive deficits, behavioral difficulties and a post-traumatic syndrome and thus it is important to understand the pathophysiology of these long-term plasticity changes after TBI. Calcium (Ca2+) has been implicated in the pathophysiology of TBI-induced neuronal death and other forms of brain injury including stroke and status epilepticus. However, the potential role of long-term changes in neuronal Ca2+ dynamics after TBI has not been evaluated. In the present study, we measured basal free intracellular Ca2+ concentration ([Ca2+]i) in acutely isolated CA3 hippocampal neurons from Sprague–Dawley rats at 1, 7 and 30 days after moderate central fluid percussion injury. Basal [Ca2+]i was significantly elevated when measured 1 and 7 days post-TBI without evidence of neuronal death. Basal [Ca2+]i returned to normal when measured 30 days post-TBI. In contrast, abnormalities in Ca2+ homeostasis were found for as long as 30 days after TBI. Studies evaluating the mechanisms underlying the altered Ca2+ homeostasis in TBI neurons indicated that necrotic or apoptotic cell death and abnormalities in Ca2+ influx and efflux mechanisms could not account for these changes and suggested that long-term changes in Ca2+ buffering or Ca2+ sequestration/release mechanisms underlie these changes in Ca2+ homeostasis after TBI. Further elucidation of the mechanisms of altered Ca2+ homeostasis in traumatized, surviving neurons in TBI may offer novel therapeutic interventions that may contribute to the treatment and relief of some of the morbidity associated with TBI.
- Publication
European Journal of Neuroscience, 2008, Vol 27, Issue 7, p1659
- ISSN
0953-816X
- Publication type
Academic Journal
- DOI
10.1111/j.1460-9568.2008.06156.x