Departamento de Histología y Anatomía, Facultad de Medicina, Universidad Miguel Hernández Alicante, Spain.
Departamento de Histología y Anatomía, Facultad de Medicina, Universidad Miguel Hernández Alicante, Spain ; Instituto de Neuroetología, Universidad Veracruzana Xalapa, Veracruz, México.
Front Neuroanat. 2015 Feb 17;9:9. doi: 10.3389/fnana.2015.00009. eCollection 2015.
Thyroid hormones are fundamental for the expression of genes involved in the development of the CNS and their deficiency is associated with a wide spectrum of neurological diseases including mental retardation, attention deficit-hyperactivity disorder and autism spectrum disorders. We examined in rat whether developmental and early postnatal hypothyroidism affects the distribution of vesicular glutamate transporter-1 (VGluT1; glutamatergic) and vesicular inhibitory amino acid transporter (VGAT; GABAergic) immunoreactive (ir) boutons in the hippocampus and somatosensory cortex, and the behavior of the pups. Hypothyroidism was induced by adding 0.02% methimazole (MMI) and 1% KClO4 to the drinking water starting at embryonic day 10 (E10; developmental hypothyroidism) and E21 (early postnatal hypothyroidism) until day of sacrifice at postnatal day 50. Behavior was studied using the acoustic prepulse inhibition (somatosensory attention) and the elevated plus-maze (anxiety-like assessment) tests. The distribution, density and size of VGluT1-ir and VGAT-ir boutons in the hippocampus and somatosensory cortex was abnormal in MMI pups and these changes correlate with behavioral changes, as prepulse inhibition of the startle response amplitude was reduced, and the percentage of time spent in open arms increased. In conclusion, both developmental and early postnatal hypothyroidism significantly decreases the ratio of GABAergic to glutamatergic boutons in dentate gyrus leading to an abnormal flow of information to the hippocampus and infragranular layers of the somatosensory cortex, and alter behavior in rats. Our data show cytoarchitectonic alterations in the basic excitatory hippocampal loop, and in local inhibitory circuits of the somatosensory cortex and hippocampus that might contribute to the delayed neurocognitive outcome observed in thyroid hormone deficient children born in iodine deficient areas, or suffering from congenital hypothyroidism.
甲状腺激素对中枢神经系统发育相关基因的表达至关重要,其缺乏与广泛的神经疾病有关,包括智力迟钝、注意力缺陷多动障碍和自闭症谱系障碍。我们在大鼠中研究了发育和早期产后甲状腺功能减退是否会影响海马体和体感皮层中囊泡谷氨酸转运体 1(VGluT1;谷氨酸能)和囊泡抑制性氨基酸转运体(VGAT;GABA 能)免疫反应性(ir)末梢的分布,以及幼鼠的行为。甲状腺功能减退症是通过在饮用水中添加 0.02%甲巯咪唑(MMI)和 1%高氯酸钾从胚胎第 10 天(E10;发育性甲状腺功能减退症)和 E21(早期产后甲状腺功能减退症)开始诱导的,直到第 50 天处死。使用声前脉冲抑制(体感注意力)和高架十字迷宫(焦虑样评估)测试来研究行为。在 MMI 幼鼠中,海马体和体感皮层中 VGluT1-ir 和 VGAT-ir 末梢的分布、密度和大小异常,这些变化与行为变化相关,因为惊跳反应幅度的前脉冲抑制减少,而开放臂的时间百分比增加。总之,发育性和早期产后甲状腺功能减退症显著降低了齿状回中 GABA 能末梢与谷氨酸能末梢的比率,导致信息异常流向海马体和体感皮层的颗粒下层,并改变了大鼠的行为。我们的数据显示,甲状腺激素缺乏的碘缺乏地区出生的儿童或患有先天性甲状腺功能减退症的儿童中观察到的神经认知延迟结果,可能与海马体基本兴奋性环路和体感皮层及海马体局部抑制回路的细胞构筑改变有关。