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首页> 外文期刊>The European Journal of Neuroscience >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.
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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.

机译：颅脑外伤会导致长期存活的钙（Ca2 +）平台，使细胞内Ca含量升高，并改变幸免于脑损伤的海马神经元的Ca2 +稳态机制。

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摘要

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.
机译：颅脑外伤（TBI）幸存者通常长期患有与认知缺陷，行为困难和创伤后综合症相关的重大发病，因此了解TBI后这些长期可塑性变化的病理生理学很重要。钙（Ca2 +）与TBI诱发的神经元死亡和其他形式的脑损伤（包括中风和癫痫持续状态）的病理生理学有关。但是，尚未评估TBI后神经元Ca2 +动态的长期变化的潜在作用。在本研究中，我们在中度中央流体敲击损伤后第1、7和30天测量了来自Sprague-Dawley大鼠的急性分离的CA3海马神经元中的基础游离细胞内Ca2 +浓度（[Ca2 +]（i））。在TBI后1天和7天测量时，基础[Ca2 +]（i）显着升高，而没有神经元死亡的证据。在TBI后30天测量时，基础[Ca2 +]（i）恢复正常。相反，TBI后长达30天才发现Ca2 +稳态异常。评估TBI神经元内Ca2 +稳态改变机制的研究表明坏死或凋亡细胞死亡以及Ca2 +内流和外排机制异常不能解释这些变化，并暗示Ca2 +缓冲或Ca2 +螯合/释放机制的长期变化是基础TBI后这些钙离子稳态的变化。进一步阐明创伤性脑损伤中幸存的神经元中Ca2 +稳态改变的机制可能会提供新颖的治疗干预措施，这些措施可能有助于治疗和缓解与创伤性脑损伤相关的某些疾病。

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