López-Sañudo S, Rodríguez-Martín E, Martín-Espinosa A, Arilla E
Departmento de Bioquímica y Biología Molecular, Facultad de Medicina, Universidad de Alcalá, Madrid, Spain.
Peptides. 1995;16(8):1453-9. doi: 10.1016/0196-9781(95)02011-x.
Somatostatin (SS) and noradrenaline (NA) are distributed in the rat cerebral cortex, and seizure activity is one of the aspects of behavior affected by both neurotransmitters. Due to the possible interaction between both neurotransmitter systems, we studied whether phenylphrine, an alpha 1-adrenoceptor agonist, and prazosin, an alpha 1-adrenoceptor antagonist, can modulate SS-like immunoreactivity (SS-LI) levels, binding of [125I][Tyr11]SS to its specific receptors, the ability of SS to inhibit adenylate cyclase (AC) activity, and the guanine nucleotide binding regulatory protein G, and G., in the Sprague-Dawley rat frontoparietal cortex. An IP dose of 2 or 4 mg/kg of phenylephrine injected 7 h before decapitation decreased the number of SS receptors and increased the apparent affinity in frontoparietal cortex membranes. An IP dose of 20 or 25 mg/kg of prazosin administered 8 h before decapitation increased the number of SS receptors and decreased their apparent affinity. The administration of prazosin before the phenylephrine injection prevented the phenylephrine-induced changes in SS binding. The addition of phenylephrine and/or prazosin 10(-5) M to the incubation medium changed neither the number nor the affinity of the SS receptors in the frontoparietal cortex membranes. Phenylephrine or prazosin affected neither SS-LI content nor the basal or forskolin (FK)-stimulated AC activities in the frontoparietal cortex. In addition, SS caused an equal inhibition of AC activity in frontoparietal cortex membranes of phenylephrine-and prazosintreated rats compared with the respective control group. Finally, phenylephrine and prazosin did not vary the pertussis toxin (PTX)-catalyzed ADP ribosylation of Gi- and/or Go-proteins. These results suggest that the above-mentioned changes are related to the phenylephrine activation of alpha 1-adrenoceptors or to the blocking of these receptors by prazosin. In addition, these data provide further support for a functional interrelationship between the alpha 1-adrenergic and somatostatinergic systems in the rat frontoparietal cortex.
生长抑素(SS)和去甲肾上腺素(NA)分布于大鼠大脑皮层,癫痫活动是受这两种神经递质影响的行为方面之一。由于这两种神经递质系统之间可能存在相互作用,我们研究了α1肾上腺素能受体激动剂去氧肾上腺素和α1肾上腺素能受体拮抗剂哌唑嗪是否能调节斯普拉格 - 道利大鼠额顶叶皮层中SS样免疫反应性(SS - LI)水平、[125I][Tyr11]SS与其特异性受体的结合、SS抑制腺苷酸环化酶(AC)活性的能力以及鸟嘌呤核苷酸结合调节蛋白G和G。断头前7小时腹腔注射2或4mg/kg去氧肾上腺素剂量可减少额顶叶皮层膜中SS受体数量并增加其表观亲和力。断头前8小时腹腔注射20或25mg/kg哌唑嗪剂量可增加SS受体数量并降低其表观亲和力。在去氧肾上腺素注射前给予哌唑嗪可防止去氧肾上腺素诱导的SS结合变化。向孵育培养基中添加10(-5)M的去氧肾上腺素和/或哌唑嗪既不改变额顶叶皮层膜中SS受体的数量也不改变其亲和力。去氧肾上腺素或哌唑嗪对额顶叶皮层中的SS - LI含量以及基础或福斯高林(FK)刺激的AC活性均无影响。此外,与各自的对照组相比,SS对去氧肾上腺素和哌唑嗪处理大鼠的额顶叶皮层膜中的AC活性具有同等程度的抑制作用。最后,去氧肾上腺素和哌唑嗪并未改变百日咳毒素(PTX)催化的Gi和/或Go蛋白的ADP核糖基化。这些结果表明上述变化与去氧肾上腺素对α1肾上腺素能受体的激活或哌唑嗪对这些受体的阻断有关。此外,这些数据为大鼠额顶叶皮层中α1肾上腺素能和生长抑素能系统之间的功能相互关系提供了进一步支持。