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Acta Physiologica 2010; Volume 200, Supplement 681
Abstracts of the 61st National Congress of the Italian Physiological Society
9/15/2010-9/17/2010
Varese, Italy
CX3CL1-INDUCED MODULATION AT CA1 SYNAPSES REVEALS MULTIPLE MECHANISMS OF EPSC MODULATION INVOLVING ADENOSINE RECEPTOR SUBTYPES
Abstract number: P76
RAGOZZINO1 D, PICCININ1 S, DI ANAGELANTONIO2 S, PICCIONI1 A, VOLPINI3 R, CRISTALLI3 G, FREDHOLM4 BB, LIMATOLA1 C, EUSEBI1 F
1Dept Physiology and Pharmacology Univ. Sapienza, Roma, Italy
2Dept Cellular and Developmental Biology Univ. Sapienza, Roma, Italy
3School of Pharmacy, Medicinal Chemistry Unit, Universit di Camerino, Italy
4Dept Physiology and Pharmacology, Karolinska Institutet, Stockolm, Sweden
We characterized the role of adenosine receptor (AR) subtypes in the modulation of glutamatergic neurotransmission by the chemokine fractalkine (CX3CL1) in mice hippocampal CA1 neurons. CX3CL1 causes a reversible depression of excitatory postsynaptic current (EPSC), abolished by the A3AR antagonist MRS1523, but not by A1AR (DPCPX) or A2AAR (SCH58261) antagonists. Consistently, CX3CL1-induced EPSC depression is absent in slices from A3AR-/- but not A1AR-/- or A2AAR-/- mice. Further, A3AR stimulation causes similar EPSC depression. In cultured neurons, CX3CL1-induced AMPA current depression shows A1AR–A3AR pharmacology. We conclude that glutamatergic depression induced by released adenosine requires the stimulation of different ARs by released adenosine
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Acta Physiologica 2010; Volume 200, Supplement 681 :P76