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.
|Titolo:||CX3CL1-induced modulation at CA1 synapses reveals multiple mechanisms of EPSC modulation involving adenosine receptor subtypes.|
|Data di pubblicazione:||2010|
|Appare nelle tipologie:||Articolo|