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| 钙/钙调素依赖性蛋白激酶Ⅱα对阿片诱导痛觉过敏大鼠中央杏仁核抑制性突触后电流的影响 |
| Effects of calcium/calmodulin-dependent kinase Ⅱα on inhibitory postsynaptic currents in central amygdala in rats with opioid induced hyperalgesia |
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| DOI：10.12089/jca.2019.06.013 |
| 中文关键词: 杏仁核 阿片 痛觉过敏 钙/钙调素依赖性蛋白激酶Ⅱα 抑制性突触后电流 |
| 英文关键词: Amygdala Opioids Hyperalgesia Calcium calmodulin-dependent protein kinase Ⅱα Inhibitory postsynaptic currents |
| 基金项目:国家自然科学基金（81771196） |
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| 摘要点击次数: 2667 |
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| 中文摘要: |
目的 探讨钙/钙调素依赖性蛋白激酶Ⅱα（CaMKⅡα）对阿片诱导痛觉过敏（OIH）大鼠中央杏仁核（CeA）抑制性突触后电流的影响。
方法 实验一：取雄性SD大鼠12只，随机分为对照组和KN93组，每组右侧CeA立体定位置管恢复1周后经颈皮下注射芬太尼（60 μg/kg×4次，间隔15 min）造OIH模型，随后对照组及KN93组大鼠CeA区分别注射50%DMSO 0.5 μl或CaMKⅡα抑制剂KN93 10 nmol，记录给药前后大鼠机械缩足反应阈（MWT）和热缩足潜伏期（TWL）。实验二：另取雄性SD大鼠32只，随机分为Con-1组、Con-2组、OIH-1组和OIH-2组，建模成功后制成脑片，其中Con-1组与OIH-1组用膜片钳记录CeA区神经元自发抑制性突触后电流（sIPSCs）；Con-2组和OIH-2组记录CeA区神经元微小抑制性突触后电流（mIPSCs），观察加用KN93 10 μmol/L前后上述电流幅值和频率的变化。
结果 实验一：与造模前比较，造模后两组MWT和TWL均明显降低（P < 0.01）；与造模后比较，给药后KN93组MWT和TWL明显升高（P<0.01）。实验二：与Con-1组比较，OIH-1组sIPSCs幅值和频率明显降低（P<0.05），给药后OIH-1组sIPSCs幅值和频率明显升高（P<0.05），但对Con-1组无明显影响；与Con-2组比较，OIH-2组mIPSCs幅值和频率亦明显降低（P<0.05），给药前后OIH-2组与Con-2组mIPSCs幅值和频率差异无统计学意义。
结论 CaMKⅡα可抑制CeA区自发抑制性突触后电流，这可能是CaMKⅡα调制阿片诱导痛觉过敏的机制之一。 |
| 英文摘要: |
Ojective To explore the effects of calcium/calmodulin-dependent protein kinase Ⅱα(CaMK Ⅱα) on inhibitory postsynaptic currents in central amygdala (CeA) in rats with opioid induced hyperalgesia (OIH).
Methods In experiment 1, 12 healthy male clean Sprague-Dawley rats, were randomly divided into 2 groups: control group and group KN93. After one-week recovery from catheterization in the right CeA, two groups were induced by fentanyl subcutaneous injection (60 μg/kg × 4, 15 min interval). Then 50% DMSO (0.5 μl) or KN93 (10 nmol/L) were administrated through the CeA catheter to control group and group KN93 accordingly. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were tested before and after OIH induction and post drug delivery through the CeA catheter. In experiment 2, another 32 healthy male clean Sprague-Dawley rats, were randomly divided into 4 groups: groups Con-1, Con-2, OIH-1 and OIH-2. OIH model was induced by previously described methods in OIH groups, same volume of saline was injected into the control groups. After success induction of OIH, brain slices were prepared, and the spontaneous inhibitory postsynaptic currents (sIPSCs) were recorded by whole-cell patch clamp in groups Con-1 and OIH-1. The miniature inhibitory postsynaptic currents (mIPSCs) were recorded in groups Con-2 and OIH-2 alternatively. Then the changes in amplitude and frequency of the IPSCs were monitored after KN93 (10 μmol/L) use.
Results Experiment 1: MWT and TWL were significantly decreased after fentanyl induction in both groups (P < 0.05). Compared with modeling, MWT and TWL in group KN93 were significantly increased (P < 0.01). Experiment 2: Compared with group Con-1, amplitude and frequency of sIPSCs in group OIH-1 were decreased significantly (P < 0.05), which could be reversed by KN93 (P < 0.05). Compared with group Con-2, amplitude and frequency of mIPSCs in group OIH-2 were decreased significantly (P < 0.05), which cant be modified by KN93.
Conclusion CaMKⅡα could inhibit the sIPSCs in the central amygdala in rats with OIH, which may contribute to the underlying mechanism of OIH. |
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