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首页> 外文期刊>Translational Stroke Research >Mild Hypothermia Suppresses Calcium-Sensing Receptor (CaSR) Induction Following Forebrain Ischemia While Increasing GABA-B Receptor 1 (GABA-B-R1) Expression
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Mild Hypothermia Suppresses Calcium-Sensing Receptor (CaSR) Induction Following Forebrain Ischemia While Increasing GABA-B Receptor 1 (GABA-B-R1) Expression

机译：轻度低体温会抑制前脑缺血后钙敏感受体（CaSR）的诱导，同时增加GABA-B受体1（GABA-B-R1）的表达

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摘要

Hypothermia improves neurological outcome from cardiac arrest. The mechanisms of protection are multifold, but identifying some may be useful in exploring potential therapeutic targets. The extracellular calcium-sensing receptor (CaSR) was originally found in parathyroid cells in which the receptor senses minute changes in extracellular [Ca2+] and promotes Ca2+ influx and intracellular Ca2+ release. The CaSR is broadly expressed in the CNS and colocalized with the inhibitory γ-aminobutyric acid-B receptor 1 (GABA-B-R1). In hippocampal neurons, GABA-B-R1 heterodimerizes with CaSR and suppresses CaSR expression. To study the interplay between these two receptors in the development of ischemic cell death and neuroprotection by hypothermia, we subjected C57/BL6 mice to global cerebral ischemia by performing bilateral carotid artery occlusion (10 min) followed by reperfusion for 1–3 days with or without therapeutic hypothermia (33°C for 3 h at the onset of reperfusion). Terminal deoxynucleotidyl transferase dUTP nick end labeling staining and immunohistochemistry showed that forebrain ischemia increased CaSR expression, decreased GABA-B-R1 expression, and promoted cell death. These changes were particularly evident in hippocampal neurons and could be reversed by mild hypothermia. The induction of CaSR, along with reciprocal decreases in GABA-B-R1 expression, may together potentiate ischemic neuronal death, suggesting a new therapeutic target for treatment of ischemic brain injury.
机译：体温过低可改善心脏骤停的神经系统预后。保护的机制是多种多样的，但确定一些机制可能有助于探索潜在的治疗靶点。细胞外钙敏感受体（CaSR）最初在甲状旁腺细胞中发现，该受体感知细胞外[Ca2 + ]的微小变化并促进Ca2 + 的流入和细胞内Ca2 + 的释放。 CaSR在CNS中广泛表达，并与抑制性γ-氨基丁酸B受体1（GABA-B-R1）共定位。在海马神经元中，GABA-B-R1与CaSR异源二聚体并抑制CaSR表达。为了研究这两种受体在低温引起的缺血性细胞死亡和神经保护作用中的相互作用，我们对C57 / BL6小鼠进行了全脑缺血，方法是进行双侧颈动脉闭塞（10分钟），然后再用或进行1至3天的再灌注无需治疗性体温过低（再灌注开始时在33°C持续3小时）。末端脱氧核苷酸转移酶dUTP缺口末端标记染色和免疫组化显示，前脑缺血可增加CaSR表达，降低GABA-B-R1表达，并促进细胞死亡。这些变化在海马神经元中尤为明显，轻度低温可以逆转。 CaSR的诱导，以及GABA-B-R1表达的相互降低，可能共同增强缺血性神经元死亡，为缺血性脑损伤的治疗提供了新的靶点。

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  • 来源
    《Translational Stroke Research》 |2011年第2期|195-201|共7页
  • 作者

    Jong Youl Kim; Nuri Kim; Midori A. Yenari; Wenhan Chang;

  • 作者单位

    Department of Neurology University of California San Francisco and Veterans Affairs Medical Center 4150 Clement St San Francisco CA 94121 USA;

    Department of Neurology University of California San Francisco and Veterans Affairs Medical Center 4150 Clement St San Francisco CA 94121 USA;

    Department of Neurology University of California San Francisco and Veterans Affairs Medical Center 4150 Clement St San Francisco CA 94121 USA;

    Department of Medicine University of California San Francisco and Veterans Affairs Medical Center San Francisco CA 94121 USA;

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  • 原文格式 PDF
  • 正文语种 eng
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  • 关键词

    Calcium-sensing receptor; Global cerebral ischemia; Hypothermia; Neuroprotection;

    机译：钙敏感受体;全脑缺血;体温过低;神经保护;

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