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目的 :研究吗啡对海马神经元 [Ca2 + ]i 影响的机制 ,为探索吗啡成瘾的神经生物学机制与可能的治疗途径。方法 :荧光探针Fluo 4标记细胞内游离钙后 ,用激光共聚焦显微镜检测吗啡对大鼠原代培养海马神经元 [Ca2 + ]i 的影响。结果 :吗啡急性刺激引起海马神经元 [Ca2 + ]i 升高 ,CTOP不能阻断吗啡引起的细胞内 [Ca2 + ]i 增加 ,而nal trindole能阻断吗啡引起的细胞内 [Ca2 + ]i 反应 ;Thapsigargin预处理阻断吗啡诱导的细胞内 [Ca2 + ]i 增加 ,Verapamil预处理不能完全抑制吗啡引起的细胞内 [Ca2 + ]i 增加 ;吗啡长时程作用后 ,海马神经元 [Ca2 + ]i 升高 ,加入纳络酮急性戒断后 ,不能阻断吗啡引起的细胞内 [Ca2 + ]i 升高 ,反而引起 [Ca2 + ]i 异常升高。结论 :吗啡急性刺激引起的海马神经元内游离钙增加主要来源于δ2 阿片受体介导的IP3 敏感的钙库释放。
OBJECTIVE: To study the mechanism of morphine on [Ca2 +] i in hippocampal neurons and to explore the neurobiological mechanisms and possible therapeutic approaches for morphine addiction. Methods: Fluorescent probe Fluo 4 labeled intracellular free calcium, laser confocal microscopy morphine on primary cultured rat hippocampal neurons [Ca2] i impact. Results: Acute morphine induced a [Ca2 +] i increase in hippocampal neurons, while CTOP failed to block intracellular [Ca2 +] i increase induced by morphine, whereas nal trindole blocked morphine-induced intracellular [Ca2 +] i response Pretreatment with Thapsigargin blocked the increase of intracellular [Ca2 +] i induced by morphine, Verapamil pretreatment could not completely inhibit the increase of intracellular [Ca2 +] i induced by morphine; After long-term morphine treatment, [Ca2 + i increased, the addition of naloxone after acute withdrawal, can not block morphine-induced intracellular [Ca2 +] i increased, but caused by abnormal increase in [Ca2 +] i. CONCLUSION: The increase of intracellular free calcium in hippocampal neurons induced by acute morphine stimulation mainly comes from the release of δ2 opioid receptor-mediated IP3-sensitive calcium stores.