4.5 Article

Traumatic brain injury causes a long-lasting calcium (Ca2+)-plateau of elevated intracellular Ca levels and altered Ca2+ homeostatic mechanisms in hippocampal neurons surviving brain injury

Journal

EUROPEAN JOURNAL OF NEUROSCIENCE
Volume 27, Issue 7, Pages 1659-1672

Publisher

WILEY
DOI: 10.1111/j.1460-9568.2008.06156.x

Keywords

acute dissociation of neuron; calcium dynamics; Fura-2/Fura-FF; Sprague-Dawley rats

Categories

Funding

  1. NINDS NIH HHS [U01 NS058213-03, R01 NS052529, R01NS051505, U01 NS058213-02, R01 NS052529-03, U01 NS058213-01, R01 NS051505-03, R01 NS051505-02, R01 NS052529-02, U01NS058213, U01 NS058213, R01 NS052529-01A2, R01 NS051505-01A2, R01NS052529, R01 NS051505] Funding Source: Medline

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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.

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