TRPC1 is a compelling ion channel mediating Ca²⁺ and Na⁺ influx, highly expressed in the brain, where its precise functions remain debated. Recent studies show TRPC1 is activated by mGluR5 in the hippocampus. Group I mGluRs play a key role in synaptic plasticity, including mGluR-LTD, which is exaggerated in conditions like Fragile X syndrome (FXS). This thesis explores the involvement of TRPC1 in mGluR5-mediated plasticity. Using a Cre-tamoxifen system, acute Trpc1 deletion in FXS mice reduced social deficits, normalized memory extinction, and abolished exaggerated mGluR-LTD. mGluR5-TRPC1 activation induces ARC expression, essential for mGluR-LTD, via eEF2K and ERK1/2 pathways. These findings contribute to understanding the role of TRPC1 in both normal and pathological conditions.