Gavish M, Weizman A, Okun F, Youdim M B
J Neurochem. 1986 Oct;47(4):1106-10. doi: 10.1111/j.1471-4159.1986.tb00727.x.
The effects of 10 days of D-thyroxine (T4) treatment on central benzodiazepine (BZ) receptors in the brain and on peripheral-type BZ binding sites in the heart, kidney, and testis of rats were studied. The experimental hyperthyroidism resulted in an increase in the density of cortical central BZ receptors, without any alteration of the affinity of the receptors to [3H]flunitrazepam. The increase in cortical central BZ receptors was also accompanied by the up-regulation of peripheral BZ binding sites in the heart, kidney, and testis. The affinity of the peripheral BZ binding sites for the ligand [3H]PK 11195 was not affected by T4 treatment in any of these three organs. The increase in the density of brain cortical central BZ receptors was less prominent than the increase in the peripheral BZ binding sites. The modulatory effect of T4 treatment on central and peripheral BZ receptors might be attributed to the direct interaction of the thyroid hormone at these sites or might reflect a physiological compensatory adaptation mechanism to thyrotoxicosis associated with hypermetabolism, anxiety, and stress.
研究了10天D-甲状腺素(T4)治疗对大鼠脑内中枢苯二氮䓬(BZ)受体以及心脏、肾脏和睾丸外周型BZ结合位点的影响。实验性甲状腺功能亢进导致皮质中枢BZ受体密度增加,而受体对[3H]氟硝西泮的亲和力未发生任何改变。皮质中枢BZ受体增加的同时,心脏、肾脏和睾丸中的外周BZ结合位点也上调。在这三个器官中,T4治疗均未影响外周BZ结合位点对配体[3H]PK 11195的亲和力。脑皮质中枢BZ受体密度的增加不如外周BZ结合位点的增加显著。T4治疗对中枢和外周BZ受体的调节作用可能归因于甲状腺激素在这些位点的直接相互作用,或者可能反映了与甲状腺毒症相关的生理代偿适应机制,甲状腺毒症与代谢亢进、焦虑和应激有关。