The role of cholecystokinin in ganglionic transmission in the guinea‐pig gall‐bladder.
The role of cholecystokinin in ganglionic transmission in the guinea‐pig gall‐bladder.
复制标题
胆囊收缩素在豚鼠胆囊神经节传递中的作用。
DOI：
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
G. Mawe
中科院分区：
文献类型：
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作者：
G. Mawe
1.采用细胞内单电极电流钳和电压钳记录技术研究胆囊收缩素（CCK）对豚鼠完整胆囊神经节的作用。2.八肽胆囊收缩素（CCK-8; 0.01 - 100 nM）增加刺激神经节间纤维束诱发的快速兴奋性突触后电位（EPSP）的振幅。在大多数情况下，在正常Krebs溶液中表现出亚阈值EPSP的神经元在CCK-8存在下激发动作电位。在低Ca 2 +/高Mg 2+溶液中，CCK-8使快速EPSP的振幅增加3倍。3. CCK-8（0.01 - 100 nM）以浓度依赖性方式增加诱发兴奋性突触后电流（EPSC）的幅度。在1.0 nM时效果最大。4.在低Ca 2 +/高Mg 2+溶液中，八肽胆囊收缩素使EPSP的量子含量增加3倍，但对量子大小没有影响。5.特异性CCK‐A受体拮抗剂MK‐329（以前称为L‐ 364，718; 1.0 nM）可逆性阻断CCK‐8对神经节传递的易化作用。然而，特异性CCK-B受体拮抗剂L-365，260（10 nM）并未改变CCK-8的突触前易化作用。6.胆囊神经元对外源性ACh的反应不受CCK-8的影响。7.通过灌流（0.001 - 100 nM）或压力微喷射（100 microM）应用CCK-8对胆囊神经元的膜电位、膜电导、动作电位或阈值没有影响。8.采用免疫组织化学法确定胆囊神经节丛内神经末梢释放肽是否可引起CCK的作用。胆囊神经节丛中未检测到CCK免疫反应性，但肠肌间神经丛和粘膜下神经丛的对照制剂中存在丰富的CCK免疫反应性。9.这些结果表明，CCK对豚鼠胆囊神经节的快速突触传递具有突触前易化作用，并且这种作用是由突触前CCK‐A受体介导的。此外，似乎这种效应通常会响应激素CCK而不是从神经末梢释放的CCK。
1. The effects of cholecystokinin (CCK) on intact guinea‐pig gall‐bladder ganglia were investigated with intracellular, single‐electrode current‐ and voltage‐clamp recording techniques. 2. Cholecystokinin octapeptide (CCK‐8; 0.01‐100 nM) increased the amplitude of the fast excitatory postsynaptic potential (EPSP) that was evoked by stimulation of interganglionic fibre tracts. In most cases, neurones that exhibited subthreshold EPSPs in normal Krebs solution fired action potentials in the presence of CCK‐8. In a low Ca2+/high Mg2+ solution, CCK‐8 caused a 3‐fold increase in the amplitude of fast EPSPs. 3. The amplitude of the evoked excitatory postsynaptic current (EPSC) was increased by CCK‐8 (0.01‐100 nM) in a concentration‐dependent manner. The effect was maximal at 1.0 nM. 4. Cholecystokinin octapeptide caused a 3‐fold increase in the quantal content of the EPSP in a low Ca2+/high Mg2+ solution, but had no effect on the quantal size. 5. The specific CCK‐A receptor antagonist, MK‐329 (formerly L‐364,718; 1.0 nM), reversibly blocked the facilitatory effect of CCK‐8 on ganglionic transmission. However, the specific CCK‐B receptor antagonist, L‐365,260 (10 nM), did not alter the presynaptic facilitatory effect of CCK‐8. 6. The response of gall‐bladder neurones to exogenously applied ACh was not modified by CCK‐8. 7. Application of CCK‐8, by superfusion (0.001‐100 nM) or by pressure microejection (100 microM), had no effect on the membrane potential, membrane conductance, action potential, or threshold of gall‐bladder neurones. 8. Immunohistochemistry was employed to determine whether the actions of CCK could be elicited by release of the peptide from nerve terminals within the ganglionated plexus of the gall‐bladder. Immunoreactivity for CCK was not detected in the ganglionated plexus of the gall‐bladder, but CCK immunoreactivity was plentiful in control preparations of intestinal myenteric and submucosal plexuses. 9. These results show that CCK has a presynaptic facilitatory effect on fast synaptic transmission in guinea‐pig gall‐bladder ganglia, and that this effect is mediated by presynaptic CCK‐A receptors. Furthermore, it appears that such an effect would normally occur in response to hormonal CCK, rather than CCK that is released from nerve terminals.
狗迷走神经切断术前后胆囊收缩素释放和作用的相关性。
影响因子：
3.8
作者：
Fried,GM;Ogden,WD;Greeley,G;Thompson,JC
通讯作者：
Thompson,JC
影响因子：
29.4
作者：
Hanyu,N;Dodds,WJ;Layman,RD;Hogan,WJ;Chey,WY;Takahashi,I
通讯作者：
Takahashi,I