甲状旁腺素和降钙素对痛觉的中枢调节作用及其机理探讨  

Study of Central Modulation Effects and its Mechanism of Parathyroid Hormone and Calcitonin on Analgesia

作　　者：左萍萍[1] 张一彬[1] 于昌东 

机构地区：[1]中国医学科学院基础医学研究所药理教研室

出　　处：《基础医学与临床》1991年第3期33-35,共3页Basic and Clinical Medicine

基　　金：国家自然科学基金

摘　　要：本文观察了脑室内注射甲状旁腺素(PTH)和降钙素(CT)对小鼠痛阈及对脑突触小体^(45)Ca摄取的彩响。结果表明,PTH(0.1U、0.4U、0.8U)均使小鼠痛阈明显降低,与此相反,CT(0.5U、1.0U、2.0U)则使小鼠痛阈显著上升,并有很好的量效关系。另外,PTH(0.5U、1.0U)明显促进脑突触小体对^(45)Ca的摄取,CT(1.0U、2.0U)则明显抑制^(45)Ca的摄取。结果提示,这两种激素可能通过影响中枢神经细胞Ca^(2+)的摄取,参与中枢的痛觉调节机制。The influences of Intracerebroventricular injection of calcium regulating hormones-parathyroid hormone (PTH) and calcitonin (CT) on pain reaction in mice and 45Ca influx in brain synaptosomes in vitro were studied. The results indicated that PTH (0.1U, 0.4U, 0.8U) decreased significantly the pain threshold, while CT(0.5U, 1.0U, 2.0U) increased clearly it. All these effects had clear relations with dosages. On the other hand, PTH could also increase but CT decrease 45Ca influx in brain synaptosomes. These suggested that the both PTH and CT may regulate pain reaction through influenceing 45Ca influx, in central neural cells.

关 键 词：痛觉 甲状旁腺素 降钙素 中枢神经 

分 类 号：R338.3[医药卫生—人体生理学]