Paternostro M A, Meisami E
Department of Physiology and Biophysics, University of Illinois, Urbana 61801.
Brain Res Dev Brain Res. 1993 Dec 17;76(2):151-61. doi: 10.1016/0165-3806(93)90203-m.
To assess the effects of early thyroid deficiency, and recovery from this condition on growth and development of olfactory epithelium (OE), male Sprague-Dawley rat pups were rendered hypothyroid by addition of propylthiouracil (PTU) to their drinking water from birth. At weaning some rats continued to receive PTU while others ere allowed to recover by withdrawal of PTU. Body weights and plasma thyroxine levels were determined in all groups. At the ages of 25, 50 and 90 days, the OE of these hypothyroid and 'recovery' rats were compared with age-matched controls for surface area, epithelial thickness, density and total number of olfactory receptor neurons, basal cells and supporting cells, using morphometric and cell counting methods. Normal rats showed marked and highly significant increases in the OE surface area and olfactory neuron number (2.6- and 2.3-folds) during the post-weaning period. In the hypothyroid rats, body growth and thyroxine levels were severely suppressed. The OE in the 25-day-old hypothyroid rats showed more than 40% reduction in surface area and cell number, compared to controls, but mean epithelial thickness and surface density of cells were unchanged. In the post-weaning hypothyroid rats, the expansion of surface area was severely retarded, and increase in cell number ceased entirely. In rats allowed to recover by PTU withdrawal, by 90 days of age, body weight and size had markedly increased but had not caught up completely; however, thyroxine levels were restored to normal and the surface area and cell number in the OE had increased in a compensatory manner, completely restoring the deficiencies in OE growth, including surface area, numbers of receptor neurons, basal cells and supporting cells. The results indicate marked growth plasticity of OE in the post-weaning rats. This pronounced ability to recover from early growth retardation contrasts with that seen in central neural structures, and indicates the great potential of OE for use as a model neural system for the study of recovery from early damage and growth retardation.
为了评估早期甲状腺功能减退及其恢复对嗅上皮（OE）生长发育的影响，从出生起就通过在雄性斯普拉格-道利大鼠幼崽的饮用水中添加丙硫氧嘧啶（PTU）使其甲状腺功能减退。断奶时，一些大鼠继续接受PTU，而另一些则通过停用PTU使其恢复。测定了所有组的体重和血浆甲状腺素水平。在25、50和90日龄时，使用形态计量学和细胞计数方法，将这些甲状腺功能减退和“恢复”大鼠的OE与年龄匹配的对照组在表面积、上皮厚度、密度以及嗅觉受体神经元、基底细胞和支持细胞的总数方面进行比较。正常大鼠在断奶后期间，OE表面积和嗅觉神经元数量显著且极显著增加（分别为2.6倍和2.3倍）。在甲状腺功能减退的大鼠中，身体生长和甲状腺素水平受到严重抑制。与对照组相比，25日龄甲状腺功能减退大鼠的OE表面积和细胞数量减少了40%以上，但平均上皮厚度和细胞表面密度未改变。在断奶后的甲状腺功能减退大鼠中，表面积的扩展严重受阻，细胞数量的增加完全停止。在通过停用PTU恢复的大鼠中，到90日龄时，体重和体型显著增加，但尚未完全赶上；然而，甲状腺素水平恢复正常，OE的表面积和细胞数量以代偿方式增加，完全恢复了OE生长的缺陷，包括表面积、受体神经元数量、基底细胞和支持细胞数量。结果表明断奶后大鼠的OE具有显著的生长可塑性。这种从早期生长迟缓中显著恢复的能力与中枢神经结构中所见的情况形成对比，表明OE作为研究早期损伤和生长迟缓恢复的模型神经系统具有巨大潜力。
