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Claudin Proteins and Neuronal Function

机译：克劳丁蛋白与神经元功能

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摘要

The identification and characterization of the claudin family of tight fiction (TJ) proteins in the late 1990s ushered in a new era for research to the molecular and cellular biology of intercellular junctions. Since that time, TJs have been studied in the contexts of many diseases including deafness, male infertility, cancer, bacterial invasion, and liver and kidney disorders. In this review, we consider the role of claudins in the nervous system focusing on the mechanisms by which TJs in glial cells are involved in neuronal function. Electrophysiological evidence suggests that claudins may operate in the central nervous system (CNS) in a manner similar to polarized epithelia. We also evaluate hypotheses that TJs are the gatekeepers of an immune-privileged myelin compartment and that TJs emerged during evolution to form major adhesive forces within the myelin sheath. Finally, we consider the implications of disrupted CNS myelin TJs in the contexts of behavioral disorders (schizophrenia) and demyelinating or hypomyelinating diseases (multiple sclerosis and the leukodystrophies), and explore evidence of a possible mechanism governing affective disorder symptoms in patients with white matter abnormalities.
机译：1990年代末期对claudin紧密小说（TJ）蛋白家族的鉴定和表征为细胞间连接的分子和细胞生物学研究开辟了一个新时代。从那时起，就在许多疾病中对TJ进行了研究，包括耳聋，男性不育，癌症，细菌入侵以及肝肾疾病。在这篇综述中，我们认为claudins在神经系统中的作用侧重于胶质细胞中TJ参与神经元功能的机制。电生理证据表明，claudins可能以类似于极化上皮的方式在中枢神经系统（CNS）中起作用。我们还评估以下假设：TJ是免疫特权的髓鞘区隔的守门人，并且TJ在进化过程中出现以在髓鞘内形成主要粘附力。最后，我们考虑了行为异常（精神分裂症）和脱髓鞘或低髓鞘疾病（多发性硬化症和白细胞营养不良）的背景下，中枢神经系统髓磷脂TJ的影响，并探讨了控制白质异常患者情感障碍症状的可能机制的证据。 。

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