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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. © 2010 Elsevier B.V.

CX3CL1-induced modulation at CA1 synapses reveals multiple mechanisms of EPSC modulation involving adenosine receptor subtypes / S., Piccinin; DI ANGELANTONIO, Silvia; A., Piccioni; R., Volpini; G., Cristalli; B. b., Fredholm; Limatola, Cristina; Eusebi, Fabrizio; Ragozzino, Davide Antonio. - In: JOURNAL OF NEUROIMMUNOLOGY. - ISSN 0165-5728. - STAMPA. - 224:1-2(2010), pp. 85-92. [10.1016/j.jneuroim.2010.05.012]

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

DI ANGELANTONIO, SILVIA;LIMATOLA, Cristina;EUSEBI, Fabrizio;RAGOZZINO, Davide Antonio
2010

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. © 2010 Elsevier B.V.
2010
adenosine a1; cells; adenosine a2; deficiency/physiology; adenosine a3; adenosine receptors; knockout; presynaptic terminals; mice; epsc; synaptic transmission; genetics/immunology; excitatory postsynaptic potentials; immunology/metabolism/ultrastructure; fractalkine; hippocampal neurons; receptor; physiology; ampa receptors; chemokines; deficiency/genetics/physiology; ca1 region; animals; immunology/metabolism; inbred c57bl; adenosine a3 receptor antagonists; neural inhibition; receptors; purinergic p1; adenosine; chemokine cx3cl1; patch-clamp techniques; organ culture techniques; adenosine a1 receptor antagonists; adenosine a2 receptor antagonists; current modulation; cultured; hippocampal
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CX3CL1-induced modulation at CA1 synapses reveals multiple mechanisms of EPSC modulation involving adenosine receptor subtypes / S., Piccinin; DI ANGELANTONIO, Silvia; A., Piccioni; R., Volpini; G., Cristalli; B. b., Fredholm; Limatola, Cristina; Eusebi, Fabrizio; Ragozzino, Davide Antonio. - In: JOURNAL OF NEUROIMMUNOLOGY. - ISSN 0165-5728. - STAMPA. - 224:1-2(2010), pp. 85-92. [10.1016/j.jneuroim.2010.05.012]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/452972
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