Atterwill C K, Reid J, Athayde C M
Mol Cell Endocrinol. 1985 May;40(2-3):149-58. doi: 10.1016/0303-7207(85)90170-4.
The effect of thyroid status on the postnatal development of the two molecular forms of Na+,K+-ATPase, distinguished kinetically on the basis of their ouabain sensitivity, was examined in rat brain. Hypothyroidism induced by PTU from day 1 postnatally significantly reduced the Na+,K+-ATPase activity in cerebellum (22-30 days) but not forebrain, whereas hyperthyroidism (T4 treatment from day 1) had no effect. The hypothyroidism-induced reduction in cerebellum was reflected by a 20-45% reduction in the activity of the alpha(+) form of Na+,K+-ATPase (high ouabain affinity) against control brains compared to a 60-70% reduction in the activity of the alpha form (low ouabain affinity). These results show that neonatally induced hypothyroidism leads to a selectively greater impairment of the ontogenesis of the activity of cerebellar alpha form of Na+,K+-ATPase. This may possibly reflect a retarded development of a selective cerebellar cell population containing predominantly the alpha form of the enzyme.
在大鼠脑中研究了甲状腺状态对两种基于哇巴因敏感性在动力学上有区别的Na⁺,K⁺-ATP酶分子形式产后发育的影响。从出生后第1天起用丙硫氧嘧啶诱导的甲状腺功能减退显著降低了小脑(22 - 30天)中的Na⁺,K⁺-ATP酶活性,但额叶皮质未受影响,而甲状腺功能亢进(从第1天起用甲状腺素治疗)则没有影响。与对照脑相比,甲状腺功能减退诱导的小脑Na⁺,K⁺-ATP酶α(+)形式(高哇巴因亲和力)活性降低20 - 45%,而α形式(低哇巴因亲和力)活性降低60 - 70%。这些结果表明,新生期诱导的甲状腺功能减退导致小脑Na⁺,K⁺-ATP酶α形式活性的个体发生选择性地受到更大损害。这可能反映了主要含有该酶α形式的选择性小脑细胞群发育迟缓。