首页> 外文期刊>The Journal of Physiology >Different G proteins mediate somatostatin-induced inward rectifier K+ currents in murine brain and endocrine cells.
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Different G proteins mediate somatostatin-induced inward rectifier K+ currents in murine brain and endocrine cells.

机译:不同的G蛋白介导生长抑素诱导的鼠脑和内分泌细胞内向整流子K +电流。

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1. Types of G proteins (G protein alpha-subunit subtypes) which mediate the activation of inward rectifier K+ currents by somatostatin (somatotrophin release-inhibiting factor, SRIF) were determined in cultured locus coeruleus neurones from newborn rats and in AtT-20 cells (a mouse pituitary cell line). 2. The whole-cell patch clamp technique was used together with injection of antibodies against pertussis toxin (PTX)-sensitive G protein alpha-subunits or with injection of antisense (or sense) oligonucleotides against these G proteins. 3. In locus coeruleus neurones, the SRIF-induced activation of inward rectifier K+ currents was inhibited by anti-G alpha i1/G alpha i2 antibody injection, but not by anti-G alpha i3 or by anti-G alpha o/G alpha i3 antibody injection, suggesting that the SRIF response is mediated through G alpha i1 and/or G alpha i2. 4. The SRIF-induced activation of the inward rectifier was suppressed in locus coeruleus neurones after injection of antisense oligonucleotides against G alpha i2, but not by injection of sense oligonucleotides against G alpha i2. Injection of antisense (or sense) oligonucleotides against G alpha i1, G alpha i3 and G alpha O (common) had no effect. These results suggest that G alpha i2 is involved in this SRIF response. 5. In AtT-20 cells, the SRIF-induced activation of inward rectifier K+ currents was suppressed by injection of anti-G alpha i3 antibody, but not by injection of anti-G alpha i1/G alpha i2 antibody. 6. The above results indicate that Gi mediates the SRIF effects on inward rectifier K+ currents. However, different subtypes of Gi are involved in the brain neurones and in the endocrine cells: Gi2 in locus coeruleus neurones and Gi3 in AtT-20 cells.
机译:1.确定了新生大鼠和AtT-20细胞中培养的促蓝斑神经元介导的生长抑素(生长激素释放抑制因子,SRIF)介导内向整流子K +电流激活的G蛋白类型(G蛋白α亚基亚型)。 (小鼠垂体细胞系)。 2.全细胞膜片钳技术与注射针对百日咳毒素(PTX)敏感的G蛋白α亚基的抗体或注射针对这些G蛋白的反义(或有义)寡核苷酸一起使用。 3.在蓝斑蓝质神经元中,SRIF诱导的内向整流器K +电流激活被抗G alpha i1 / G alpha i2抗体注射抑制,但不受抗G alpha i3或抗G alpha o / G alpha抑制。 i3抗体注射,表明SRIF反应是通过G alpha i1和/或G alpha i2介导的。 4.在注射针对Gα12的反义寡核苷酸后,在蓝绿色斑点神经元中抑制了SRIF诱导的向内整流子的激活,但是没有注射针对Gα12的有义寡核苷酸。注射针对G alpha i1,G alpha i3和G alpha O(常见)的反义(或有义)寡核苷酸无效。这些结果表明,G alpha i2参与了此SRIF响应。 5.在AtT-20细胞中,SRIF诱导的向内整流器K +电流的激活可通过注射抗G alpha i3抗体来抑制,但不能通过注射抗G alpha i1 / G alpha i2抗体来抑制。 6.以上结果表明,Gi可调节SRIF对内向整流器K +电流的影响。但是,Gi的不同亚型与大脑神经元和内分泌细胞有关:蓝斑脑神经元中的Gi2和AtT-20细胞中的Gi3。

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