Abbasian Mohammad, Sayyah Mohammad, Babapour Vahab, Mahdian Reza
Department of Physiology, Faculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.
Basic Clin Neurosci. 2013 Fall;4(4):334-40.
Gap junctions are intercellular membrane channels that provide direct cytoplasmic continuity between adjacent cells. This communication can be affected by changes in expression of gap junctional subunits called Connexins (Cx). Changes in the expression and function of connexins are associated with number of brain neurodegenerative diseases. Neuroinflammation is a hallmark of various central nervous system (CNS) diseases, like multiple sclerosis, Alzheimer's disease and epilepsy. Neuroinflammation causes change in Connexins expression. Hippocampus, one of the main brain regions with a wide network of Gap junctions between different neural cell types, has particular vulnerability to damage and consequent inflammation. Cx32 - among Connexins- is expressed in hippocampal Olygodandrocytes and some neural subpopulations. Although multiple lines of evidence indicate that there is an association between neuroinflammation and the expression of connexin, the direct effect of neuroinflammation on the expression of connexins has not been well studied. In the present study, the effect of neuroinflammation induced by the Lipopolysaccharide (LPS) on Cx32 gene and protein expressions in rat hippocampus is evaluated.
LPS (2.5µg/rat) was infused into the rat cerebral ventricles for 14 days. Cx32 mRNA and protein levels were measured by Real Time PCR and Western Blot after 1st, 7th and 14th injection of LPS in the hippocampus.
Significant increase in Cx32 mRNA expression was observed after 7th injection of LPS (P < 0.001). However, no significant change was observed in Cx32 protein level.
LPS seems to modify Cx32 GJ communication in the hippocampus at transcription level but not at translation or post-translation level. In order to have a full view concerning modification of Cx32 GJ communication, effect of LPS on Cx32 channel gating should also be determined.
间隙连接是细胞间的膜通道，可在相邻细胞之间提供直接的细胞质连续性。这种通讯可能会受到称为连接蛋白（Cx）的间隙连接亚基表达变化的影响。连接蛋白表达和功能的变化与多种脑部神经退行性疾病有关。神经炎症是各种中枢神经系统（CNS）疾病的标志，如多发性硬化症、阿尔茨海默病和癫痫。神经炎症会导致连接蛋白表达发生变化。海马体是大脑的主要区域之一，不同神经细胞类型之间存在广泛的间隙连接网络，特别容易受到损伤并随之发生炎症。在连接蛋白中，Cx32在海马少突胶质细胞和一些神经亚群中表达。尽管有多项证据表明神经炎症与连接蛋白的表达之间存在关联，但神经炎症对连接蛋白表达的直接影响尚未得到充分研究。在本研究中，评估了脂多糖（LPS）诱导的神经炎症对大鼠海马体中Cx32基因和蛋白表达的影响。
将LPS（2.5μg/大鼠）注入大鼠脑室，持续14天。在海马体首次、第7次和第14次注射LPS后，通过实时PCR和蛋白质印迹法测量Cx32 mRNA和蛋白水平。
第7次注射LPS后，观察到Cx32 mRNA表达显著增加（P < 0.001）。然而，Cx32蛋白水平未观察到显著变化。
LPS似乎在转录水平而非翻译或翻译后水平改变海马体中的Cx32间隙连接通讯。为了全面了解Cx32间隙连接通讯的改变，还应确定LPS对Cx32通道门控的影响。
