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机构地区:[1]解放军农牧大学基础部,吉林长春130062 [2]白求恩医科大学,吉林长春130021
出 处:《中国兽医学报》1999年第6期584-587,共4页Chinese Journal of Veterinary Science
摘 要:运用电生理学技术和心血管实验,观察了中央杏仁核(CeA)神经元与孤束核(NTS)神经元活动之间的相互作用,以及在CeA 内注射地塞米松(Dex)对NTS内去甲肾上腺素(NA)/神经肽Y(NPY)诱导的心血管效应的影响。电生理学实验显示,用L-谷氨酸兴奋CeA 神经元后,NTS内神经元活动主要呈现抑制反应(12/18);向NTS内注射NPY 后,CeA 内神经元活动也以抑制反应为主(13/23)。向CeA 内注射Dex,可以消除NTS内微量注射NA/NPY 所引起的降压和减慢心率效应。NA:动脉血压下降(- 0.37±0.25) kPa,心率下降(- 5±5) 次/m in,对照分别为(- 2.57±0.21) kPa,(- 33±11) 次/m in。NPY:(- 0.47±0.29)kPa,(- 10±8) 次/m in,对照(- 3.37±0.36) kPa, (- 50±9) 次/m in。由此表明,不仅CeA 与NTS在心血管活动调节中存在相互抑制作用,而且当CeA 受到高水平的糖皮质激素作用时,会抑制NTS内降压系统的作用。The interactions between the activities of neurones in central amygdaloid nucleus (CeA) and nucleus tractus solitarii (NTS), and the effect of dexamethasone (Dex) microinjected into CeA on cardiovascular response to NA/NPY administrated into NTS were observed. 12 of 18 neurone discharges in NTS were inhibited after CeA being stimulated by L glutamate.13 of 23 neurone discharges in CeA were also inhibited after microinjection of neuropeptide Y (NPY) into NTS. Microinjection of Dex (40 ng) into CeA could abolish the depressor response to NA/NPY administrated into NTS(NA: (-0.37±0.25) kPa, (-5±5) beats/min VS control (-2.57±0.21) kPa, (-33±11) beats/min; NPY: (-0.47±0.29) kPa, (-10±8) beats/min VS control (-3.37±0.36) kPa, (-50±9) beats/min. The results showed that there were inhibitory interactions between the neurons in CeA and NTS and the depressor effect of NTS could be inhibited after CeA being affected by high level of glucocorticoid . It might be an important factor responsible for hypertension induced by stress.
分 类 号:R338.26[医药卫生—人体生理学]
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