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硫酸化胆囊收缩素八肽(CCK-8)对迷走神经背核的影响。

Effects of sulphated cholecystokinin octapeptide (CCK-8) on the dorsal motor nucleus of the vagus.

作者信息

Plata-Salamán C R, Fukuda A, Oomura Y, Minami T

机构信息

Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

出版信息

Brain Res Bull. 1988 Nov;21(5):839-42. doi: 10.1016/0361-9230(88)90054-8.

Abstract

Sulphated cholecystokinin octapeptide (CCK-8) was applied by superfusion (2.1 x 10(-7) to 4.2 x 10(-6) M) to neurons of the dorsal motor nucleus of the vagus (DMV) in slice preparations of the rat medulla oblongata. Intracellular recordings show 23 of 54 (43%) neurons to be depolarized and the depolarization to be associated with an increase in membrane input resistance; 6 of 54 (11%) neurons were hyperpolarized and the hyperpolarization was associated with a decrease in membrane input resistance. Both effects were dose-dependent, reversible and persisted after blockade of synaptic transmission by Ca2+ free/high Mg2+ solution. On the other hand, nonsulphated CCK-8, a nonactive analogue of CCK-8, had no effect. These data show that vagal neurons in the DMV have receptors for CCK-8 and that CCK-8 may modulate vagal output mainly by increasing neuronal excitability.

摘要

将硫酸化胆囊收缩素八肽(CCK - 8)通过灌流法(浓度为2.1×10⁻⁷至4.2×10⁻⁶M)施加于大鼠延髓切片标本中迷走神经背核(DMV)的神经元上。细胞内记录显示,54个神经元中有23个(43%)出现去极化,且这种去极化与膜输入电阻增加有关;54个神经元中有6个(11%)出现超极化,且这种超极化与膜输入电阻降低有关。两种效应均呈剂量依赖性、可逆性,并且在无钙/高镁溶液阻断突触传递后仍持续存在。另一方面,CCK - 8的无活性类似物——非硫酸化CCK - 8则无此作用。这些数据表明,DMV中的迷走神经神经元具有CCK - 8受体,并且CCK - 8可能主要通过增加神经元兴奋性来调节迷走神经输出。

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