Systemic cholecystokinin differentially affects baro-activated GABAergic neurons in rat caudal ventrolateral medulla.

Systemic cholecystokinin differentially affects baro-activated GABAergic neurons in rat caudal ventrolateral medulla.
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全身胆囊收缩素对大鼠尾侧腹外侧髓质中气压激活的 GABA 能神经元有不同的影响。

DOI:
10.1152/jn.00526.2006
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发表时间:
2006
影响因子:
2.5
通讯作者:
Schreihofer,AnnM
Schreihofer,AnnM
中科院分区:
医学3区
文献类型:
--
作者:
Mobley,SusanC;Mandel,DanielA;Schreihofer,AnnM

文献摘要

被引文献

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胆囊收缩素(CCK)在饭后释放,以促进消化和饱腹感。循环CCK抑制内脏交感神经活动(sSNA),这可能有助于餐后肠系膜血流量增加。CCK诱导的交感神经抑制通过激活迷走传入神经和抑制前交感头端腹外侧延髓(RVLM)神经元的一个子集而发生。本研究旨在确定尾侧延髓腹外侧区(CVLM)是否也可能在CCK诱导的sSNA变化中发挥作用。用氯醛糖麻醉大鼠,人工通气,麻痹,并准备记录动脉压(AP),心率(HR),sSNA和单个CVLM神经元的活性。静脉注射CCK-8(8-10 μg/kg)可降低sSNA、AP和HR,其中25个压力激活的CVLM神经元被CCK兴奋(增加3.4倍),其余7个压力激活的CVLM神经元不受影响(n= 7)或被抑制(n= 3)。通过GAD 67 mRNA的存在,确认了被激活(n= 8)或未受影响(n= 2)的压力激活的CVLM神经元的子集是GABA能的。通过微量注射蝇蕈醇对CVLM的双侧抑制将sSNA和AP的降低逆转为显著的交感神经激活和AP的增加(n= 18)。这些数据表明,全身注射CCK导致大多数压力激活的GABA能CVLM神经元的激活,CVLM是必不可少的CCK诱导的抑制sSNA的生产。压力激活的GABA能CVLM神经元对CCK的不同反应可能有助于用系统CCK观察到的RVLM前交感神经元和交感流出的不同反应。
Cholecystokinin (CCK) is released after a meal to promote digestion and satiety. Circulating CCK inhibits splanchnic sympathetic nerve activity (sSNA), which may contribute to postprandial increases in mesenteric blood flow. The CCK-induced sympathoinhibition occurs by activation of vagal afferent nerves and inhibition of a subset of presympathetic rostral ventrolateral medullary (RVLM) neurons. The present study sought to determine whether the caudal ventrolateral medulla (CVLM) may also play a role in the CCK-induced changes in sSNA. Rats were anesthetized with chloralose, artificially ventilated, paralyzed, and prepared for recording arterial pressure (AP), heart rate (HR), sSNA, and activity of individual CVLM neurons. Injection of CCK-8 (8–10 μg/kg, iv) decreased sSNA, AP, and HR. Most baro-activated CVLM neurons were excited by CCK (n= 25, 3.4-fold increase), whereas other baro-activated CVLM neurons were not affected (n= 7) or were inhibited (n= 3). A subset of baro-activated CVLM neurons that were activated (n= 8) or unaffected (n= 2) was confirmed to be GABAergic by the presence of GAD67 mRNA. Bilateral inhibition of the CVLM by microinjections of muscimol reversed the decreases in sSNA and AP to a prominent sympathoactivation and increase in AP (n= 18). These data suggest that systemic injection of CCK leads to the activation of most baro-activated GABAergic CVLM neurons and that the CVLM is essential for the production of CCK-induced inhibition of sSNA. The differential responses of baro-activated GABAergic CVLM neurons to CCK may contribute to the diverse responses of presympathetic RVLM neurons and sympathetic outflows observed with systemic CCK.