Effect of hypo- and hyperthyroidism on hexokinase in the developing cerebellum of the rat.
Effect of hypo- and hyperthyroidism on hexokinase in the developing cerebellum of the rat.
复制标题
甲状腺功能减退和甲状腺功能亢进对大鼠小脑发育中己糖激酶的影响。
DOI：
10.1111/j.1471-4159.1981.tb00431.x
复制
发表时间：
1981
影响因子：
4.7
通讯作者：
Wilson,JE
中科院分区：
文献类型：
--
作者：
Gutekunst,DI;Wilson,JE
在对照组、甲状腺功能减退和甲状腺功能亢进大鼠的小脑发育过程中，测量了总己糖激酶水平(单位/克组织)。此外，还用免疫荧光方法观察了己糖激酶在发育中的小脑中的分布。甲状腺功能减退症延迟了正常情况下出生后总己糖激酶活性的增加，而甲状腺功能亢进症则加速了这种增加。在正常动物中，成熟的Purkinje细胞中己糖激酶的水平经历了一过性的升高，在出生后大约8天达到最高水平，然后在12天后迅速下降到相对较低的水平；甲状腺功能减退症延缓了这种短暂的增加和随后的下降，但甲状腺功能亢进症似乎没有明显影响这种现象的发生时间。根据其强烈的荧光判断，小脑肾小球的己糖激酶含量相对丰富。甲状腺功能减退症延缓了浓染肾小球的发育。甲亢似乎不会导致肾小球数量的早熟增加，但可能增加了己糖激酶被新形成的肾小球同化的速度。甲状腺功能减退和甲亢对小脑总己糖激酶水平的影响从甲状腺激素对富含己糖激酶的突触结构的生化成熟的影响来解释。
Total hexokinase levels (units/g tissue) have been measured during postnatal development of the cerebellum in control, hypothyroid, and hyperthyroid rats. In addition, distribution of hexokinase in the developing cerebellum has been observed with an immunofluorescence method. Hypothyroidism delays the normally observed postnatal increase in total hexokinase activity, whereas hyperthyroidism accelerates the increase. In normal animals, hexokinase levels in maturing Purkinje cells pass through a transient increase, with maximal levels at approximately 8 days postnatally followed by rapid decline to relatively low levels by 12 days; hypothyroidism delays this transient increase and subsequent decline, but hyperthyroidism does not appear to affect markedly the timing of this phenomenon. Cerebellar glomeruli are relatively enriched in hexokinase content, as judged by their intense fluorescence. Hypothyroidism delays the development of intensely stained glomeruli. Hyperthyroidism did not appear to cause precocious increase in numbers of glomeruli but may have increased the rate at which the hexokinase was assimilated by newly formed glomeruli. The effects of hypo‐ and hyperthyroidism on total cerebellar hexokinase levels are interpreted in terms of the effect of thyroid hormone on the biochemical maturation of synaptic structures rich in hexokinase.