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首页> 外文期刊>American Journal of Physiology >Role of glutamate in the rostral ventrolateral medulla in acupuncture-related modulation of visceral reflex sympathoexcitation.
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Role of glutamate in the rostral ventrolateral medulla in acupuncture-related modulation of visceral reflex sympathoexcitation.

机译:谷氨酸在延髓腹侧延髓在针刺内脏反射交感神经兴奋相关调节中的作用。

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摘要

Visceral sympathoexcitatory reflexes induced by stimulation of the gallbladder with bradykinin (BK) are attenuated by electroacupuncture (EA) at Neiguan-Jianshi (P5-6) acupoints located over the median nerve. Previous studies have shown that neurons in the rostral ventrolateral medulla (rVLM) receive convergent input from visceral organs and somatic nerves (activated by EA). Glutamate (Glu), an important excitatory neurotransmitter in the rVLM, processes visceral sympathoexcitatory cardiovascular reflexes. In the present study, we determined the relation between EA-mediated opioidergic modulation of visceral cardiovascular responses and Glu. Reflex cardiovascular responses were evoked by application of BK to the gallbladder before and after EA in anesthetized cats. Glu concentrations ([Glu]) were measured by HPLC from samples collected by microdialysis probe(s) inserted unilaterally or bilaterally into the rVLM. BK-induced reflex responses and [Glu] were attenuated by 45% and 70%, respectively, after 30 min of EA (n = 6). EA alone did not change [Glu] in the rVLM (n = 6, P > 0.05). However, microdialysis of naloxone (100 mM) into the rVLM reversed EA-related inhibition of blood pressure and [Glu] (n = 5). Immunohistochemical visualization showed that delta-opioid receptors colocalized with, and were in close apposition to, vesicular Glu transporter 3- and c-Fos-double-labeled perikarya and processes of rVLM neurons after gallbladder stimulation with BK. These data suggest that EA attenuates BK-induced visceral sympathoexcitatory reflexes through opioid-mediated inhibition of Glu's action in the rVLM.
机译:由缓激肽(BK)刺激胆囊引起的内脏交感兴奋反射通过位于中枢神经上方的内关结石(P5-6)穴位的电针(EA)减弱。先前的研究表明,延髓腹侧延髓(rVLM)中的神经元从内脏器官和躯体神经(由EA激活)接收收敛的输入。谷氨酸(Glu)是rVLM中重要的兴奋性神经递质,可引起内脏交感兴奋性心血管反射。在本研究中,我们确定了EA介导的内脏心血管反应的阿魏酸调节与Glu之间的关系。在麻醉的猫中,EA之前和之后,在胆囊中应用BK会引起反射性心血管反应。通过HPLC从单侧或双侧插入rVLM的微透析探针收集的样品中测量Glu浓度([Glu])。 EA 30分钟后(n = 6),BK诱导的反射反应和[Glu]分别减弱了45%和70%。单独的EA并没有改变rVLM中的[Glu](n = 6,P> 0.05)。但是,纳洛酮(100 mM)在rVLM中的微渗析逆转了EA相关的血压和Glu抑制作用(n = 5)。免疫组织化学可视化显示,δ-阿片受体与BK胆囊刺激后与囊泡Glu转运蛋白3-和c-Fos-双标记的周核细胞共定位,并紧密并列,并与rVLM神经元的过程有关。这些数据表明,EA通过阿片类药物介导的rVLM中Glu的抑制作用减弱了BK诱导的内脏交感兴奋反射。

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