Leung F C, Saggerson E D, Clark J B
Department of Biochemistry and Molecular Biology, University College London, UK.
Dev Neurosci. 1996;18(3):153-61. doi: 10.1159/000111404.
The abundances of G protein alpha-subunits (Gi1 alpha, Gi2 alpha, G0 alpha and Gq/ll alpha) were measured in synaptosomal membranes isolated from forebrain and hindbrain regions of euthyroid and hypothyroid neonatal rats at 10, 15, 20 and 25 days post-partum. The findings show that hypothyroidism causes a distinct perturbation of the normal developmental profile of these signalling components. It is suggested that these changes may contribute to some of the neurological deficits arising from hypothyroidism in early development.
在产后10、15、20和25天，测量了从甲状腺功能正常和甲状腺功能减退的新生大鼠的前脑和后脑区域分离出的突触体膜中G蛋白α亚基（Gi1α、Gi2α、G0α和Gq/11α）的丰度。研究结果表明，甲状腺功能减退会对这些信号成分的正常发育模式造成明显干扰。有人提出，这些变化可能是早期发育中甲状腺功能减退引起的一些神经功能缺陷的原因。
