Chemokine- and neurotransmitter-receptor crosstalk in myelin-producing cells

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Abstract

Multiple sclerosis (MS) manifests as acute focal demyelination and axonal loss with limited repair. Different extent of repair in demyelinating plaques can be due to the presence of variety of reactive inflammatory cells as well as apoptotic oligodendrocytes. Among different suggested modes for pathological heterogeneity observed in MS, primary oligodendrocyte degeneration is observed in the majority of patients. In addition, the expression of chemokine- as well as glutamatergic-receptors on oligodendrocytes have already been shown by several studies. Data showed the over-expression of chemokines in the vicinity of inflammatory and/or neurodegenerative diseases of CNS. Moreover, studies suggested that glutamate excess during the process of inflammation can cause excitotoxicity and oligodendrocyte death. In this study, the patch-clamp technique was used to investigate the effect of CXCL1 chemokine-receptor interaction on kinetics of oligodendrocyte glutamatergic receptor. This study demonstrates for the first time that chemokine~receptor interaction can alter the kinetic of the glutamate receptor channel in myelin producing cells. The modulatory effects of applied chemokine were completely hampered, using an antagonist. In conclusion, the result of this study may open a new window to achieve a better understanding of pathogenesis of demyelinating diseases such as MS andmay suggest a potential role for chemokines in glutamate excitotoxicity.

Keyword(s)

CXCL1; Chemokine; Glutamate; Progenitor; Whole cell patch-clamp

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