Binge drinking (BD) is characterized by consuming at least 70 g for men and 56 g for women of pure alcohol within two hours. Clinical studies examining the impact of BD on memory in young adults have revealed impairments across various types of memory (episodic, visuospatial, working memory...), although the frequency of BD often varies among studies. Preclinical research indicates that BD leads to the degradation of glutamate-dependent synaptic plasticity, the cellular mechanism of learning and memory in the hippocampus, including the metabotropic form of glutamatergic long-term synaptic depression (mGlu1/5-LTD). However, it remains unclear whether and how different frequencies of BD alter mGlu1/5-LTD. Therefore, we investigated whether high and low frequencies of BD in rats produce distinct effects on mGlu1/5-LTD, and we explored the involvement of mTOR, an early modulated target of ethanol, as a potential factor in our findings. Male rats (P30 – P35) received 8 intraperitoneal injections of ethanol (3g/kg, 20% v/v) or saline over 7 days (High Frequency “HF” group) or 14 days (Low Frequency “LF” group). Three days after ethanol exposure, using hippocampal slices, mGlu1/5-LTD was abolished in the HF group and potentiated in the LF group. Bath application of rapamycin (1µM), an mTOR inhibitor, restored mGlu1/5-LTD in the LF group only, suggesting that low frequency BD increases mGlu1/5-LTD through mTOR activation. We conclude that BD frequency differently affects synaptic plasticity in the hippocampus through distinct pathways and should likely be considered in clinical studies to differentiate memory impairments between binge drinkers and heavy binge drinkers.