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首页> 美国卫生研究院文献>British Journal of Pharmacology and Chemotherapy >Cellular actions of somatostatin on rat periaqueductal grey neurons in vitro
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Cellular actions of somatostatin on rat periaqueductal grey neurons in vitro

机译：生长抑素在体外对大鼠导水管周围灰色神经元的细胞作用

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Functional studies indicate that the midbrain periaqueductal grey (PAG) is involved in the analgesic actions of somatostatin; however, the cellular actions of somatostatin in this brain region are unknown. In the present study, whole-cell patch clamp recordings were made from rat PAG neurons in vitro. In 93% of acutely isolated neurons, somatostatin inhibited Ca2+-channel currents. This effect was mimicked by the sst-2 selective agonist BIM-23027, but not by the sst-1 and sst-5 selective agonists CH-275 and L-362855. In brain slices, 81% of neurons responded to somatostatin (300 nM) with an increase in K+ conductance that reversed polarity at −114 mV. A greater proportion of somatostatin-sensitive neurons (93%) than somatostatin-insensitive neurons (53%) responded to the opioid agonist met-enkephalin (10 μM). Somatostatin also reduced the amplitude of evoked GABAA-mediated inhibitory postsynaptic currents (IPSCs). The actions of somatostatin in brain slices were mimicked by BIM-23027, but not by CH-275. Somatostatin had a variable effect on the rate of spontaneous miniature IPSCs in normal external potassium solutions. In high external potassium solutions, somatostatin reduced the rate of miniature IPSCs in all neurons, and this inhibition was abolished by addition of Cd2+ (30 μM). Somatostatin had no effect on the amplitude of miniature IPSCs. These results indicate that somatostatin acts via sst-2 receptors to directly inhibit a subpopulation of PAG neurons by activating a potassium conductance and inhibits GABA release within PAG via a presynaptic Ca2+-dependent mechanism. Thus, like opioids, somatostatin has the potential to exert pre- and postsynaptic disinhibitory effects within the PAG.
机译：功能研究表明，中脑导水管周围灰色（PAG）与生长抑素的镇痛作用有关。然而，生长抑素在该大脑区域的细胞作用尚不清楚。在本研究中，全细胞膜片钳记录是从大鼠PAG神经元体外制备的。在93％的急性分离神经元中，生长抑素抑制Ca 2 + 通道电流。 sst-2选择性激动剂BIM-23027模仿了这种作用，但sst-1和sst-5选择性激动剂CH-275和L-362855则没有。在脑片中，有81％的神经元对生长抑素（300 nM）作出反应，其K + 电导增加，在-114 mV时极性相反。对阿片类激动剂甲脑啡肽（10μM）的反应，对生长抑素敏感的神经元（93％）的比例高于对生长抑素不敏感的神经元（53％）的比例。生长抑素还降低了诱发的GABAA介导的抑制性突触后电流（IPSC）的幅度。 BIM-23027模仿了脑切片中生长抑素的作用，而CH-275则没有。生长抑素对正常外部钾溶液中自发微型IPSC的发生率具有可变影响。在高外部钾溶液中，生长抑素降低了所有神经元中微型IPSC的比率，并且通过添加Cd 2 + （30μM）消除了这种抑制作用。生长抑素对微型IPSC的振幅没有影响。这些结果表明，生长抑素通过sst-2受体通过激活钾电导来直接抑制PAG神经元的亚群，并通过突触前Ca 2 + 依赖性机制抑制PAG内GABA的释放。因此，与阿片类药物一样，生长抑素也有可能在PAG中发挥突触前和突触后的抑制作用。

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