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Updated: Jun 12, 2026

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology
Published on: April 23, 2019
CX3CL1-induced modulation at CA1 synapses reveals multiple mechanisms of EPSC modulation involving adenosine receptor
S Piccinin1, S Di Angelantonio, A Piccioni
1Istituto Pasteur-Fondazione Cenci Bolognetti & Dipartimento di Fisiologia e Farmacologia Sapienza Università di Roma, Piazzale A. Moro 5, 00185 Rome, Italy.
Abstract:
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. 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, CX3CL1-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.
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