摘要
目的评价芬太尼诱发大鼠痛觉过敏时伤害性杏仁核兴奋性突触增强的机制与杏仁核基底外侧核和臂旁核通路的关系。方法清洁级健康雄性SD大鼠32只,体重80~100 g,采用随机数字表法分为2组(n=16):对照组(C组)和痛觉过敏组(H组)。H组颈部皮下注射芬太尼60μg/kg(浓度为50μg/ml),共注射4次,每次给药间隔15 min,诱发大鼠痛觉过敏;C组给予等容量生理盐水(1.2 ml/kg)。分别于给予芬太尼前和给予芬太尼后6.5 h时测定机械缩足反应阈(MWT)和热缩足潜伏期(TWL)。然后处死大鼠,制备同时包含伤害性杏仁核和杏仁核基底外侧核及同时包含伤害性杏仁核和臂旁核投射区的脑片,采用双电极膜片钳技术,将刺激电极分别置于杏仁核基底外侧核或臂旁核投射区,记录电极置于伤害性杏仁核神经元,记录钙/钙调素依赖性蛋白激酶Ⅱα抑制剂KN93(10μmol/L)灌流前后刺激诱发的兴奋性突触后电流(eEPSCs)幅值。结果与给予芬太尼前比较,2组给予芬太尼后6.5 h时MWT降低,TWL缩短(P<0.01);与加入KN93前比较,H组加入KN93后杏仁核基底外侧核-伤害性杏仁核神经元和臂旁核-伤害性杏仁核神经元eEPSCs幅值降低(P<0.01);与C组比较,H组给予芬太尼后6.5 h时MWT升高,TWL延长,加入KN93前杏仁核基底外侧核-伤害性杏仁核神经元和臂旁核-伤害性杏仁核神经元eEPSCs幅值升高(P<0.01)。结论芬太尼诱发大鼠痛觉过敏时,伤害性杏仁核兴奋性突触增强既来源于杏仁核基底外侧核又来源于臂旁核传入,且CaMKⅡα对这两种来源的突触传递都有调节作用。
Objective To evaluate the relationship between the mechanism underlying excitatory synaptic potentiation in nociceptive amygdala and basolateral amygdala(BLA)and parabrachial pathways in a rat model of sufentanil-induced hyperalgesia.Methods Thirty-two healthy clean-grade male Sprague-Dawley rats,weighing 80-100 g,were divided into 2 groups(n=16 each)using a random number table method:control group(C group)and hyperalgesia group(H group).Hyperalgesia was induced by subcutaneous injection of fentanyl 60μg/kg(concentration 50μg/ml)for 4 times at a 15-min interval in group H.The equal volume of normal saline 1.2 ml/kg was given instead in group C.The mechanical paw withdrawal threshold(MWT)and thermal paw withdrawal latency(TWL)were measured before giving fentanyl and at 6.5 h after giving fentanyl.Animals were then sacrificed,and brain slices containing nociceptive amygdala and BLA and brain slices containing nociceptive amygdala and projection area of parabrachial nuclei(PBN)were prepared.The stimulating electrodes were placed in the BLA or projection area of PBN,and the recording electrodes were placed in the nociceptive amygdala neurons,using the two-electrode patch-clamp technique.The amplitude of evoked excitatory postsynaptic currents(eEPSCs)induced by stimulation was recorded before and after perfusing with Ca^2+/calmodulin-dependent protein kinase IIα(CaMKⅡα)antagonist KN93(10μmol/L).Results Compared with the baseline before giving fentanyl,the MWT was significantly decreased and TWL was shortened at 6.5 h after giving fentanyl in two groups(P<0.01).The amplitude of eEPSCs in BLA-and PBN-nociceptive amygdala neurons was significantly lower after adding KN93 than before adding KN93 in group H(P<0.01).Compared with group C,the MWT was significantly increased and TWL was prolonged at 6.5 h after giving fentanyl,and the amplitude of eEPSCs in BLA-and PBN-nociceptive amygdala neurons was increased before adding KN93 in group H(P<0.01).Conclusion Excitatory synaptic potentiation in nociceptive amygdala ori
作者
王希希
盛晴宇
罗放
Wang Xixi;Sheng Qingyu;Luo Fang(Department of Anesthesiology,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China)
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2019年第12期1468-1471,共4页
Chinese Journal of Anesthesiology
基金
国家自然科学基金(81771196)。
关键词
芬太尼
痛觉过敏
杏仁核
突触传递
基底外侧核
臂旁核
Fentanyl
Hyperalgesia
Amygdala
Synaptic transmission
Basolateral nuclear complex
Parabrachial nucleus
