کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5736476 1613771 2017 44 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Phencyclidine-induced dysregulation of primary cilia in the rodent brain
ترجمه فارسی عنوان
اختلال قاعده سلولی اولیه در مغز جوندگان ناشی از فنسیکیدیدین
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب (عمومی)
چکیده انگلیسی
Significant roles of the primary cilia in the central nervous system have been reported in neural generation and cognitive functions. However, little is known about the possible pathological changes in brain primary cilia in neuropsychiatric disorders. To obtain an insight into the relationship between cilial dysregulation and schizophrenia, we presently investigated the effects of psychotomimetics, phencyclidine, MK-801 (dizocilpine), and methamphetamine, on morphological and molecular indices in the rodent brain. Using an immunohistochemical technique, we found that a subcutaneous injection of phencyclidine, an NMDA type glutamate receptor (NMDAR) antagonist, caused a reduction in the long axis length of a primary cilium in the CA1 region of the hippocampus without affecting that in the dentate gyrus and medial prefrontal cortex of rats and mice. The region-selective modulation of primary cilia was mimicked by another NMDAR antagonist, MK-801, but not by the indirect dopamine agonist methamphetamine. Furthermore, systemic administration of phencyclidine, but not methamphetamine, down-regulated mRNA expression of primary cilium morphology-related genes, including kif3a, 5-HTR6, RPGRIP1L, and TMEM67, and of genes composing the cilial Wnt/β-catenin signaling pathway, β-catenin, syn2 and Bcl-2, in the hippocampus, but not in the cerebral cortex of rats. These findings suggest that NMDAR hypofunction-induced dysregulation of CA1 primary cilia could be involved in the pathophysiology of dopamine transmission-independent symptoms of schizophrenia.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1674, 1 November 2017, Pages 62-69
نویسندگان
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