CX₃CL1-induced modulation at CA1 synapses reveals multiple mechanisms of EPSC modulation involving adenosine receptor subtypes

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• 作者：S. Piccinin ; S. Di Angelantonio ; A. Piccioni ; R. Volpini ; G. Cristalli ; B.B. Fredholm ; C. Limatola ; F. Eusebi ; D. Ragozzino
• 关键词：AMPA receptors ; Hippocampal neurons ; Adenosine ; Adenosine receptors ; Chemokines ; Current modulation ; Fractalkine ; EPSC
• 刊名：Journal of Neuroimmunology
• 出版年：2010
• 出版时间：27 July 2010
• 年：2010
• 卷：224
• 期：1-2
• 页码：85-92
• 全文大小：884 K

文摘

We characterized the role of adenosine receptor (AR) subtypes in the modulation of glutamatergic neurotransmission by the chemokine fractalkine (CX₃CL1) in mouse hippocampal CA1 neurons. CX₃CL1 causes a reversible depression of excitatory postsynaptic current (EPSC), which is abolished by the A₃R antagonist MRS1523, but not by A₁R (DPCPX) or A_2AR (SCH58261) antagonists. Consistently, CX₃CL1-induced EPSC depression is absent in slices from A₃R^−/− but not A₁R^−/− or A_2AR^−/− mice. Further, A₃R stimulation causes similar EPSC depression. In cultured neurons, CX₃CL1-induced depression of AMPA current shows A₁R–A₃R pharmacology. We conclude that glutamatergic depression induced by released adenosine requires the stimulation of different ARs.