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

S. Piccinin, S. Di Angelantonio, A. Piccioni, R. Volpini, G. Cristalli, B. B. Fredholm, C. Limatola, F. Eusebi, D. Ragozzino

Research output: Contribution to journalArticlepeer-review

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. CX3CL1 causes a reversible depression of excitatory postsynaptic current (EPSC), which is abolished by the A3R antagonist MRS1523, but not by A1R (DPCPX) or A2AR (SCH58261) antagonists. Consistently, CX3CL1-induced EPSC depression is absent in slices from A3R-/- but not A1R-/- or A2AR-/- 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.

Original languageEnglish
Pages (from-to)85-92
Number of pages8
JournalJournal of Neuroimmunology
Volume224
Issue number1-2
DOIs
Publication statusPublished - Jul 2010

Keywords

  • Adenosine
  • Adenosine receptors
  • AMPA receptors
  • Chemokines
  • Current modulation
  • EPSC
  • Fractalkine
  • Hippocampal neurons

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

Fingerprint Dive into the research topics of 'CX3CL1-induced modulation at CA1 synapses reveals multiple mechanisms of EPSC modulation involving adenosine receptor subtypes'. Together they form a unique fingerprint.

Cite this