Ter-Markosian A S, Lutsenko V K, Khudaverdian D N, Khlebnikova N N
Biull Eksp Biol Med. 1987 Oct;104(10):402-4.
Ca2+ blood serum level was reduced by 34.5% in rats with hypoparathyroidism (HPT) on the 7th-12th day after the damage of parathyroid glands. Synaptosomes isolated from the brain cortex of rats during this period accumulated in a normal medium more 45Ca2+ than synaptosomes from healthy animals. In potassium depolarization, control and experimental synaptosomes accumulated more 45Ca2+, however in HPT the increment in 45Ca2+ uptake in high potassium medium was less temperature-dependent. In normal medium 3H-GABA uptake and release by synaptosomes from the brain of rats with HPT slightly differed from those in the control. On the contrary, 3H-GABA release induced by synaptosome depolarization was depressed in HPT. It is suggested that nerve terminal excretory function disturbances contribute to increased excitability of the central nervous system in hypoparathyroidism.
甲状旁腺损伤后第7至12天,甲状旁腺功能减退(HPT)大鼠的血清Ca2+水平降低了34.5%。在此期间,从大鼠大脑皮层分离出的突触体在正常培养基中比健康动物的突触体积累了更多的45Ca2+。在钾去极化过程中,对照和实验突触体积累了更多的45Ca2+,然而在HPT中,高钾培养基中45Ca2+摄取的增加对温度的依赖性较小。在正常培养基中,HPT大鼠大脑突触体对3H-GABA的摄取和释放与对照略有不同。相反,突触体去极化诱导的3H-GABA释放在HPT中受到抑制。提示神经末梢排泄功能障碍导致甲状旁腺功能减退时中枢神经系统兴奋性增加。