دوره 9، شماره 2 - ( March & April 2018 1396 )                   جلد 9 شماره 2 صفحات 129-134 | برگشت به فهرست نسخه ها


XML English Abstract Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Moradi M, Saidijam M, Yadegarazari R, Jahangard L, Seifi M, Matinnia N et al . Genes Encoding GABA-β and HT1D Receptors in Bipolar I (Manic Phase) Patients. BCN. 2018; 9 (2) :129-134
URL: http://bcn.iums.ac.ir/article-1-814-fa.html
Genes Encoding GABA-β and HT1D Receptors in Bipolar I (Manic Phase) Patients. مجله علوم اعصاب پایه و بالینی. 1396; 9 (2) :129-134

URL: http://bcn.iums.ac.ir/article-1-814-fa.html


چکیده:  

Introduction: According to the cumulative evidence, genes encoding GABA receptors inhibit neurotransmitters in CNS and are intricately involved in the pathogenesis of mood disorders. Based on this hypothesis, these genes may be expressed in bipolar patients. As a result, we evaluated the gene expressions of GABA-β3 and HT1D receptors to assess their associations with bipolar mood disorder. 
Methods: In this study, 22 patients with bipolar I disorder (single manic episode) and 22 healthy individuals were enrolled. All participants were older than 15 years and had referred to Farshchian Hospital, Hamadan, Iran. They were diagnosed based on DSM IV–TR criteria and young mania rating scale in order to determine the severity of mania by a psychiatrist as bipolar Type 1 disorder in manic episode.  We evaluated the expression of GABA–β3 and HT1D receptor genes in peripheral blood mononuclear cells, using  real-time RT-PCR analysis.
Results: In our study, a reduction in the gene expression of GABA–β3 and HT1D receptors was observed in peripheral blood mononuclear cells of the patients with bipolar disorders compared to the healthy controls.
Conclusion: The results of this study supports the hypothesis that the gene expression for serotonin and GABA receptors can be employed  in elucidating the pathogenesis of bipolar disorders.

نوع مطالعه: Original | موضوع مقاله: Clinical Neuroscience
دریافت: ۱۳۹۵/۵/۲۵ | پذیرش: ۱۳۹۶/۳/۲۸ | انتشار: ۱۳۹۶/۱۲/۱۲

فهرست منابع
1. Arisoy, O., & Oral, E. T. (2009). [Genetic studies of bipolar disorder: a review (Turkish)]. Turkish Journal of Psychiatry, 20(3), 282-293. [PMID]
2. Barnett, J. H., & Smoller, J. W. (2009). The genetics of bipolar disorder. Neuroscience, 164(1), 331-43. doi: 10.1016/j.neuroscience.2009.03.080. [DOI:10.1016/j.neuroscience.2009.03.080]
3. Bas, A., Forsberg, G., Hammarström, S., & Hammarström, M. L. (2004). Utility of the Housekeeping Genes 18S rRNA, β-Actin and Glyceraldehyde-3-Phosphate-Dehydrogenase for Normalization in Real-Time Quantitative Reverse Transcriptase-Polymerase Chain Reaction Analysis of Gene Expression in Human T Lymphocytes. Scandinavian Journal of Immunology, 59(6), 566-573. doi: 10.1111/j.0300-9475.2004.01440.x [DOI:10.1111/j.0300-9475.2004.01440.x]
4. Charych, E. I., Liu, F., Moss, S. J., & Brandon, N. J. (2009). GABA(A) receptors and their associated proteins: Implications in the etiology and treatment of schizophrenia and related disorders. Neuropharmacology, 57(5-6), 481-95. doi: 10.1016/j.neuropharm.2009.07.027 [DOI:10.1016/j.neuropharm.2009.07.027]
5. Cruceanu, C., Alda, M., Rouleau, G., & Turecki, G. (2011). Response to treatment in bipolar disorder. Current Opinion in Psychiatry, 24(1), 24-28. doi: 10.1097/YCO.0b013e328341352c [DOI:10.1097/YCO.0b013e328341352c]
6. Domschke, K. (2013). Clinical and Molecular Genetics of Psychotic Depression. Schizophrenia Bulletin, 39(4), 766-75. doi: 10.1093/schbul/sbt040 [DOI:10.1093/schbul/sbt040]
7. English, D., & Andersen, B. R. (1974). Single-step separation of red blood cells, granulocytes and mononuclear leukocytes on discontinuous density gradients of Ficoll-Hypaque. Journal of Immunological Methods, 5(3), 249-252. doi: 10.1016/0022-1759(74)90109-4 [DOI:10.1016/0022-1759(74)90109-4]
8. Fatemi, S. H., Folsom, T. D., Rooney, R. J., & Thuras, P. D. (2013). Expression of GABAA α2-, β1- and receptors are altered significantly in the lateral cerebellum of subjects with schizophrenia, major depression and bipolar disorder. Translational Psychiatry, 3(9), e303–e303. doi: 10.1038/tp.2013.6 [DOI:10.1038/tp.2013.6]
9. Gonzalez-Burgos, G., Fish, K. N., & Lewis, D. A. (2011). GABA neuron alterations, cortical circuit dysfunction and cognitive deficits in schizophrenia. Neural Plasticity, 2011, 2723184. doi: 10.1155/2011/723184 [DOI:10.1155/2011/723184]
10. Luscher, B., Shen, Q., & Sahir, N. (2010). The GABAergic deficit hypothesis of major depressive disorder. Molecular Psychiatry, 16(4), 383-406. doi: 10.1038/mp.2010.120 [DOI:10.1038/mp.2010.120]
11. Mohler, H. (2012). The GABA system in anxiety and depression and its therapeutic potential. Neuropharmacology, 62(1), 42-53. doi: 10.1016/j.neuropharm.2011.08.040 [DOI:10.1016/j.neuropharm.2011.08.040]
12. Mundo, E., Zai, G., Lee, L., Parikh, S. V., & Kennedy, J. L. (2001). The 5HT1Dβ Receptor Gene in Bipolar Disorder: A Family-based Association Study. Neuropsychopharmacology, 25(4), 608-13. doi: 10.1016/S0893-133X(01)00259-7 [DOI:10.1016/S0893-133X(01)00259-7]
13. Somogyi, P., Tamas, G., Lujan, R., & Buhl, E. H. (1998). Salient features of synaptic organisation in the cerebral cortex. Brain Research Reviews, 26(2-3), 113-35. doi: 10.1016/s0165-0173(97)00061-1 [DOI:10.1016/S0165-0173(97)00061-1]
14. Wu, C., & Sun, D. (2015). GABA receptors in brain development, function, and injury. Metabolic Brain Disease, 30(2), 367-79. doi: 10.1007/s11011-014-9560-1 [DOI:10.1007/s11011-014-9560-1]

ارسال نظر درباره این مقاله : نام کاربری یا پست الکترونیک شما:
CAPTCHA code

کلیه حقوق این وب سایت متعلق به Basic and Clinical Neuroscience می باشد.

طراحی و برنامه نویسی : یکتاوب افزار شرق

© 2018 All Rights Reserved | Basic and Clinical Neuroscience

Designed & Developed by : Yektaweb