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

被引:37
作者
Piccinin, S. [2 ,3 ]
Di Angelantonio, S. [1 ,4 ]
Piccioni, A. [2 ,3 ]
Volpini, R. [5 ]
Cristalli, G. [5 ]
Fredholm, B. B. [6 ]
Limatola, C. [2 ,3 ,7 ]
Eusebi, F. [2 ,3 ,7 ]
Ragozzino, D. [2 ,3 ]
机构
[1] Univ Roma La Sapienza, Dipartimento Biol Cellulare & Sviluppo, I-00185 Rome, Italy
[2] Univ Roma La Sapienza, Ist Pasteur, Fdn Cenci Bolognetti, I-00185 Rome, Italy
[3] Univ Roma La Sapienza, Dipartimento Fisiol & Farmacol, I-00185 Rome, Italy
[4] Univ Roma La Sapienza, Ctr Res Neurobiol Daniel Bovet, I-00185 Rome, Italy
[5] Univ Camerino, Sch Pharm, Med Chem Unit, I-62032 Camerino, MC, Italy
[6] Karolinska Inst, Dept Physiol & Pharmacol, S-17177 Stockholm, Sweden
[7] Neuromed IRCCS, I-86077 Pozzilli, IS, Italy
关键词
AMPA receptors; Hippocampal neurons; Adenosine; Adenosine receptors; Chemokines; Current modulation; Fractalkine; EPSC; SYNAPTIC-TRANSMISSION; A(3) RECEPTORS; CHEMOKINE RECEPTORS; GLUCOSE DEPRIVATION; RAT-BRAIN; FRACTALKINE; NEURONS; A(1); ACTIVATION; NEUROTOXICITY;
D O I
10.1016/j.jneuroim.2010.05.012
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We characterized the role of adenosine receptor (AR) subtypes in the modulation of glutamatergic neurotransmission by the chemokine fractalkine (CX(3)CL1) in mouse hippocampal CA1 neurons. CX(3)CL1 causes a reversible depression of excitatory postsynaptic current (EPSC), which is abolished by the A(3)R antagonist MRS1523, but not by A(1)R (DPCPX) or A(2A)R (SCH58261) antagonists. Consistently, CX(3)CL1-induced EPSC depression is absent in slices from A(3)R(-/-) but not A(1)R(-/-) or A(2A)R(-/-) mice. Further, A(3)R stimulation causes similar EPSC depression. In cultured neurons. CX3CL1-induced depression of AMPA current shows A(1)R-A(3)R pharmacology. We conclude that glutamatergic depression induced by released adenosine requires the stimulation of different ARs. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:85 / 92
页数:8
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