Somatostatin blocks a calcium current in rat sympathetic ganglion neurones.
Somatostatin blocks a calcium current in rat sympathetic ganglion neurones.
复制标题
生长抑素阻断大鼠交感神经节神经元中的钙电流。
DOI：
10.1113/jphysiol.1989.sp017494
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
G. Schofield
中科院分区：
文献类型：
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作者：
S. Ikeda;G. Schofield
1.使用膜片钳技术的全细胞变体研究了生长抑素和生长抑素类似物对急性分离和短期（24 - 48 h）培养的成年大鼠上级颈神经节（SCG）神经元的Ca 2+电流的影响。2. [D-Trp 8]生长抑素（SOM）可快速、可逆和浓度依赖性地降低Ca 2+电流。在-15 mV至+40 mV的电压范围内，Ca 2+电流幅度降低，幅度最大时（约+10 mV）降低幅度最大。在SOM存在下，Ca 2+电流上升相缓慢，在0 ~+40 mV电位范围内为双相。3.应用0.1 microM-SOM超过10 s导致反应脱敏。在施加0.1 microM-SOM的4分钟期间，Ca 2+电流幅度恢复到对照的约90%。第二次应用0.1 microM-SOM产生的块比初始应用少。4. SOM、生长抑素-14（SOM-14）和生长抑素-28（SOM-28）的浓度响应曲线拟合为单位点结合等温线。SOM、SOM-14和SOM-28产生Ca 2+电流半最大阻断和最大可达阻断的浓度分别为3.3、5.4和35 nM，分别为55、51和54%。SOM-14和SOM-28以类似于SOM的方式减慢Ca 2+电流上升阶段。生长抑素-28在1 μ M时对Ca 2+电流没有影响。5.在存在1 μ M咪唑克生、阿托品、纳洛酮或生长抑素拮抗剂氨基庚酰-Phe-D-Trp-Lys-O-苄基-Thr的情况下，0.1 μ M SOM产生的Ca 2+电流阻滞幅度没有显著改变。6.使用含有500 μ M-鸟苷酰-亚氨二磷酸（Gpp（NH）p）或鸟苷-5 '-O-（3-硫代三磷酸）（GTP-γ-S）的溶液进行内部透析，分别使Ca 2+电流幅度降低36%和41%，并诱导Ca 2+电流的双相上升相。在这些条件下，与对照组相比，0.1 microM-SOM的应用产生的Ca 2+电流振幅阻滞显著减少（分别为7.1%和14.7%）。7.使用含有500 μ M-鸟苷-5 '-O-（2-硫代二磷酸）（GDP-β-S）的溶液进行内部透析，对0.1 μ M-SOM产生的Ca 2+电流幅度或阻滞没有显著影响。8.使用含有500 μ M环腺苷3 '，5'-单磷酸（环AMP）和3-异丁基-1-甲基黄嘌呤的溶液进行内部透析，对0.1 μ M SOM产生的Ca 2+电流阻滞或Ca 2+电流幅度均无显著影响。（400字处截断摘要）
1. The effects of somatostatin and somatostatin analogues on a Ca2+ current from acutely isolated and short‐term (24‐48 h) cultured adult rat superior cervical ganglion (SCG) neurones were studied using the whole‐cell variant of the patch‐clamp technique. 2. [D‐Trp8]Somatostatin (SOM) produced a rapid, reversible and concentration‐dependent reduction of the Ca2+ current. Ca2+ current amplitude was reduced over the voltage range ‐15 to +40 mV with the greatest reduction occurring where the amplitude was maximal (ca +10 mV). In the presence of SOM, the Ca2+ current rising phase was slower and biphasic at potentials between 0 and +40 mV. 3. Application of 0.1 microM‐SOM for greater than 10 s resulted in a desensitization of the response. During a 4 min application of 0.1 microM‐SOM, Ca2+ current amplitude returned to about 90% of control. A second application of 0.1 microM‐SOM produced less block than the initial application. 4. Concentration‐response curves for SOM, somatostatin‐14 (SOM‐14) and somatostatin‐28 (SOM‐28) were fitted to a single‐site binding isotherm. The concentrations producing half‐maximal block and the maximal attainable blocks of the Ca2+ current for SOM, SOM‐14 and SOM‐28 were 3.3, 5.4 and 35 nM, respectively and 55, 51 and 54%, respectively. SOM‐14 and SOM‐28 slowed the Ca2+ current rising phase in a manner similar to that of SOM. Somatostatin‐28 had no effect on the Ca2+ current at 1 microM. 5. The magnitude of the Ca2+ current block produced by 0.1 microM‐SOM was not significantly altered in the presence of 1 microM‐idazoxan, atropine, naloxone or the somatostatin antagonist aminoheptanoyl‐Phe‐D‐Trp‐Lys‐O‐benzyl‐Thr. 6. Internal dialysis with solutions containing 500 microM‐guanylyl‐imidodiphosphate (Gpp(NH)p) or guanosine‐5'‐O‐(3‐thiotriphosphate)(GTP‐gamma‐S) decreased the Ca2+ current amplitude by 36 and 41%, respectively, and induced a biphasic rising phase in the Ca2+ current. Under these conditions, application of 0.1 microM‐SOM produced significantly less block of Ca2+ current amplitude (7.1 and 14.7%, respectively) when compared with controls. 7. Internal dialysis with solutions containing 500 microM‐guanosine‐5'‐O‐(2‐thiodiphosphate)(GDP‐beta‐S) had no significant effect on either the Ca2+ current amplitude or block produced by 0.1 microM‐SOM. 8. Internal dialysis with solutions containing 500 microM‐cyclic adenosine 3',5'‐monophosphate (cyclic AMP) and 3‐isobutyl‐1‐methylxanthine had no significant effect on either the Ca2+ current block produced by 0.1 microM‐SOM or the Ca2+ current amplitude.(ABSTRACT TRUNCATED AT 400 WORDS)