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我们以前的实验证明,大鼠或小鼠经束缚应激10h后,血清中出现一类淋巴细胞转化抑制因子。它的产生依赖于中枢神经系统的活动。本研究主要观察中枢神经系统中γ-氨基丁酸(GABA)能神经元在应激后血清淋巴细胞转化抑制因子产生中的作用。结果表明,给小鼠腹腔注射 GABA 降解酶抑制剂氨氧乙酸(AOAA,25mg/kg),升高脑内GABA 含量后,几乎完全阻断应激后血清中淋巴细胞转化抑制因子的产生。安定可增强GABA 与 GABA_A 受体的亲和性,给小鼠腹腔注射安定20mg/kg,应激后血清淋巴细胞转化抑制因子的产生也有明显降低。相反,注射 GABA 合成和释放抑制剂3-巯基丙酸(3-MP 24mg/kg),降低脑内GABA能神经元功能,可加强应激后血清淋巴细胞转化抑制因子的产生。以上实验结果从正、反两方面说明应激时脑内GABA能神经元具有对抗血清淋巴细胞转化抑制因子产生的作用。
Our previous experiments demonstrated that a class of lymphocyte transformation inhibitory factor appeared in serum after 10 hours of restraint stress in rats or mice. Its production depends on the activities of the central nervous system. This study mainly focused on the role of γ-aminobutyric acid (GABA) neurons in the central nervous system (CNS) in the generation of repressor of serum lymphocytes after stress. The results showed that intraperitoneal injection of GABA-degrading enzyme inhibitor AOAA (25 mg / kg) and intraperitoneal injection of GABA increased the production of lymphocyte transforming inhibitory factor (IL-10) in the serum almost completely after stress. Diazepam enhances the affinity of GABA and GABA_A receptor. After intraperitoneal injection of 20mg / kg diazepam, diazepam could significantly reduce the production of serum lymphocyte transformation inhibitory factor. In contrast, injection of 3-mercaptopropionic acid (3-MP 24 mg / kg), a GABA synthesis and release inhibitor, reduced the function of GABAergic neurons in the brain and enhanced the production of repressor of serum lymphocyte transformation after stress. The above experimental results from the positive and negative aspects of stress GABAergic neurons in the brain have the role of anti-serum lymphocyte transformation inhibitory factor.