N6-methyladenosine (m6A) methylation, the most prevalent eukaryotic mRNA modification, is enriched in the mammalian brain and the synaptic transcriptome. m6A methylation is dynamically regulated by enzymes called m6A writers (METTL3/14) and erasers (FTO), that are present in distal neuronal processes. Although recent studies link dynamic m6A methylome changes during synaptic plasticity to memory consolidation, the exact mechanisms in neuronal circuits remain unclear. This study investigates m6A methylation effects on synaptic transmission and plasticity within hippocampal networks, utilizing pharmacological tools to modulate the m6A machinery.The effects of m6A targeting drugs (C4-METTL3 activator, C3- FTO inhibitor, STM2457-METTL3 inhibitor, 1µM ) on synaptic function were investigated using extracellular recordings in area CA1 of rat hippocampal slices at two developmental stages (P14 and P90). Synaptic m6A methylated RNAs were visualized using immunohistochemistry, after intraperitoneal administration of the drugs (1 mg/kg). Results indicate that m6A methylated RNAs were detectable in pre/post-synaptic compartments, with levels significantly increased following METTL3/14 activator (C4) or FTO inhibitor (C3) application. Electrophysiological assessments showed that inhibition of METTL3 by STM2457 blocked Long term potentiation (LTP) induction both in juveniles and adults, without affecting basal synaptic transmission. Pharmacologically induced increase in m6A methylation affected synaptic transmission in a developmentally regulated manner. Interestingly, an increase in postsynaptic m6A methylation, induced by C3 or C4, correlated with loss of LTP as well as attenuated Long term depression. In conclusion, our findings demonstrate m6A methylation's crucial role in regulating hippocampal synaptic plasticity, suggesting potential therapeutic avenues for memory disorders.