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首页> 外文期刊>Thyroid: official journal of the American Thyroid Association >Hypothyroidism in the adult rat causes incremental changes in brain-derived neurotrophic factor, neuronal and astrocyte apoptosis, gliosis, and deterioration of postsynaptic density
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Hypothyroidism in the adult rat causes incremental changes in brain-derived neurotrophic factor, neuronal and astrocyte apoptosis, gliosis, and deterioration of postsynaptic density

机译：成年大鼠甲状腺功能减退症会导致脑源性神经营养因子，神经元和星形胶质细胞凋亡，神经胶质增生和突触后密度下降的增量变化

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Background: Adult hypothyroidism is a highly prevalent condition that impairs processes, such as learning and memory. Even though tetra-iodothyronine (T 4) treatment can overcome the hypothyroidism in the majority of cases, it cannot fully recover the patient's learning capacity and memory. In this work, we analyzed the cellular and molecular changes in the adult brain occurring with the development of experimental hypothyroidism. Methods: Adult male Sprague-Dawley rats were treated with 6-propyl-2-thiouracil (PTU) for 20 days to induce hypothyroidism. Neuronal and astrocyte apoptosis were analyzed in the hippocampus of control and hypothyroid adult rats by confocal microscopy. The content of brain-derived neurotrophic factor (BDNF) was analyzed using enzyme-linked immunosorbent assay (ELISA) and in situ hybridization. The glutamatergic synapse and the postsynaptic density (PSD) were analyzed by electron microscopy. The content of PSD proteins like tyrosine receptor kinase B (TrkB), p75, and N-methyl-d-aspartate receptor (NMDAr) were analyzed by immunoblot. Results: We observed that the hippocampus of hypothyroid adult rats displayed increased apoptosis levels in neurons and astrocyte and reactive gliosis compared with controls. Moreover, we found that the amount of BDNF mRNA was higher in the hippocampus of hypothyroid rats and the content of TrkB, the receptor for BDNF, was reduced at the PSD of the CA3 region of hypothyroid rats, compared with controls. We also observed that the glutamatergic synapses from the stratum radiatum of CA3 from hypothyroid rats, contained thinner PSDs than control rats. This observation was in agreement with a reduced content of NMDAr subunits at the PSD in hypothyroid animals. Conclusions: Our data suggest that adult hypothyroidism affects the hippocampus by a mechanism that alters the composition of PSD, reduces neuronal and astrocyte survival, and alters the content of the signaling neurotrophic factors, such as BDNF.
机译：背景：成人甲状腺功能减退症是一种高度流行的疾病，会损害诸如学习和记忆等过程。即使在大多数情况下四碘甲状腺素（T 4）治疗可以克服甲状腺功能减退症，但它不能完全恢复患者的学习能力和记忆力。在这项工作中，我们分析了随着实验性甲状腺功能减退症的发展，成人大脑中细胞和分子的变化。方法：成年雄性Sprague-Dawley大鼠用6-丙基-2-硫尿嘧啶（PTU）治疗20天，以诱发甲状腺功能减退。共聚焦显微镜分析了成年大鼠和甲状腺功能减退大鼠海马神经元和星形胶质细胞的凋亡。使用酶联免疫吸附测定（ELISA）和原位杂交技术分析了脑源性神经营养因子（BDNF）的含量。用电子显微镜分析谷氨酸能突触和突触后密度（PSD）。通过免疫印迹分析了酪氨酸受体激酶B（TrkB），p75和N-甲基-d-天冬氨酸受体（NMDAr）等PSD蛋白的含量。结果：我们观察到，与对照组相比，甲状腺功能减退的成年大鼠海马表现出神经元和星形胶质细胞凋亡水平增加以及反应性神经胶质增生。此外，我们发现，与对照组相比，甲状腺功能减退大鼠海马中BDNF mRNA的含量更高，并且在甲状腺功能减退大鼠CA3区的PSD处，BDNF受体TrkB的含量降低。我们还观察到，来自甲状腺功能减退大鼠的CA3放射状层的谷氨酸能突触所包含的PSDs比对照大鼠薄。该观察结果与甲状腺机能减退动物中PSD的NMDAr亚基含量降低是一致的。结论：我们的数据表明，成人甲状腺功能减退症通过改变PSD的成分，减少神经元和星形胶质细胞存活以及改变信号性神经营养因子（如BDNF）的含量来影响海马。

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