目的研究反复给予甲基安非它明对大鼠蓝斑至海马投射纤维去甲肾上腺素类神经递质释放的影响。方法甲基安非它明组大鼠给予小剂量甲基安非它明(5mg/kg,腹腔注射,qd,持续7 d),对照组大鼠等量生理盐水处理7 d,停药1 d后,电刺激麻醉大鼠蓝斑核团,碳纤维电极恒流安培法实时记录海马CA1区递质释放。结果与对照组相比,甲基安非它明组大鼠体重下降,刻板行为评分增加;电刺激蓝斑核团,海马CA1区递质释放信号的达峰时间延长(2.1±0.5 s vs 1.4±0.2 s,n=6,P<0.05),峰值下降(134.3±79.1 pA vs 328.7±130.7 pA,n=6,P<0.05),半衰时间减少(5.9±1.6 s vs 10.3±4.1 s,n=6,P<0.05),致使海马区域释放的递质减少。结论 7 d给予甲基安非它明减少了蓝斑至海马投射区域递质的释放,可能与甲基安非它明神经毒性作用机制有关。
Objective To study the dynamic characteristics of norepinephrine(NE)release in hypothalamus followed by electrical stimulation in locus coeruleus in the rat model of stress-inducedhypertension(SIH)and explore the role...
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Objective To study the dynamic characteristics of norepinephrine(NE)release in hypothalamus followed by electrical stimulation in locus coeruleus in the rat model of stress-inducedhypertension(SIH)and explore the role of angiotensin type 2 receptor in the pathogenesis of *** 44 rats were randomly divided into control(n=20)and stress groups(n=24).The hypertension model was established by combining noise and foot-shock *** the end of modeling,NE release in the hypothalamus by electrical stimulation in locus coeruleus was studied and NE signal was recorded by carbon fiber *** peak value,the time to peak and half-life period of NE signal in both group rats were *** The peak value of NE signal in the hypothalamic followed by electrical stimulation in locus coeruleus in SIH rats were more than in controls(P<0.01).Intraperitoneal injection of PD123,319(AT2 receptor antagonist)potentiated electrical stimulation in locus coeruleus induced NE release in the hypothalamus in SIH rats and elevated blood pressure(P<0.05),whereas intracerebroventricular injection of CGP42112(AT2 receptor agonist)inhibited the NE release and reduced the heart rate(P<0.05).Conclusions Combining noise and foot-shock stresses increased the secretion of NE in the hypothalamus followed by electrical stimulation in locus coeruleus in *** type 2 receptor plays an inhibition effect on NE release in hypothalamus in SIH *** findings suggest that angiotensin type 2 receptor can be a pharmacology target for treatment of SIH.
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