Adenosine A_2A receptor inhibition reduces synaptic and cognitive hippocampal alterations in Fmr1 KO mice.

ABSTRACT: In fragile X syndrome (FXS) the lack of the fragile X mental retardation protein (FMRP) leads to exacerbated signaling through the metabotropic glutamate receptors 5 (mGlu5Rs). The adenosine A_2A receptors (A_2ARs), modulators of neuronal damage, could play a role in FXS. A synaptic colocalization and a strong permissive interaction between A_2A and mGlu5 receptors in the hippocampus have been previously reported, suggesting that blocking A_2ARs might normalize the mGlu5R-mediated effects of FXS. To study the cross-talk between A_2A and mGlu5 receptors in the absence of FMRP, we performed extracellular electrophysiology experiments in hippocampal slices of Fmr1 KO mouse. The depression of field excitatory postsynaptic potential (fEPSPs) slo

SUBMITTER: Ferrante A 

PROVIDER: S-EPMC7864914 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature