کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
9414630 1292050 2005 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Congenital hypothyroidism alters the phosphorylation of ERK1/2 and p38MAPK in the hippocampus of neonatal rats
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب تکاملی
پیش نمایش صفحه اول مقاله
Congenital hypothyroidism alters the phosphorylation of ERK1/2 and p38MAPK in the hippocampus of neonatal rats
چکیده انگلیسی
Thyroid hormone deficiency during the critical period of neural differentiation produces permanent and severe alterations in the morphology and function of the nervous system leading to cretinism. Perinatal hypothyroidism results in permanent alterations of hippocampal synaptic functions in adult rats consequently causing learning and memory impairment. Mitogen-activated protein kinases (MAPKs) are a family of protein kinases that regulate essential cellular activities ranging from gene expression, mitosis, programmed cell death to plasticity and memory formation, but their involvement in perinatal hypothyroidism is not determined. The present work was designed to investigate MAPKs phosphorylation in hippocampus of congenital neonatal hypothyroid rats. Congenital hypothyroidism promotes an increase in extracellular signal-regulated kinases 1/2 (ERK 1/2) phosphorylation (+50%) and a decrease in p38MAPK phosphorylation (−50%) without changing in Jun N-terminal kinases (JNK) phosphorylation. Therefore, the congenital hypothyroidism model disturbs ERK 1/2 and p38MAPK phosphorylation pathways causing an important molecular alteration in the hippocampus. This event might be related, at least partially, to the deficits in hippocampal development and cognitive functions due neonatal congenital hypothyroidism.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Developmental Brain Research - Volume 154, Issue 1, 1 January 2005, Pages 141-145
نویسندگان
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