Although diverse stimulation patterns induce excitatory plasticity, they concurrently trigger long-term potentiation (iLTP) or depression (iLTD) at inhibitory synapses. Nevertheless, the precise plasticity rules and molecular mechanisms governing the interaction between excitatory and GABAergic plasticity remain unclear. Here, we aimed to elucidate these mechanisms in slices by simultaneously recording excitatory and distinct optogenetically evoked inhibitory postsynaptic currents in hippocampal CA1 pyramidal cells (CA1PCs). Long-term plasticity was induced by NMDA treatment.Our experiments revealed heterosynaptic crosstalk between excitatory and inhibitory plasticity. A 2min30s NMDA infusion induced excitatory LTD concurrent with iLTP in SST→PC input, while shorter administrations led to simultaneous expression of eLTP and iLTP in all analysed inputs. Furthermore, manipulation of distinct components of extracellular matrix selectively affected GABAergic plasticity in specific projections. Brain chondroitin digestion impaired specifically SST→PC iLTP, whereas hyaluronan digestion hindered PV→PC iLTP induction. Additionally, we explored the role of integrins in crosstalk between excitatory and inhibitory synapses. Activation of β3-integrins with fibrinogen potentiated excitatory and inhibitory SST inputs to CA1PC but depressed the PV pathway. In contrast, inhibition of β3-integrin-dependent adhesion depressed both analyzed inhibitory drives but left excitatory input intact. Finally, we demonstrated the critical dependence of iLTP maintenance on transsynaptic interaction between neuroligin-2 and neurexin. Peptide blocking this adhesion abolished already induced GABAergic plasticity. In summary, these findings reveal the intricate plasticitome of CA1PCs and underscore the crucial roles of extracellular matrix, integrins, and neuroligin-2 in molecular mechanisms of local crosstalk between excitatory and inhibitory synapses and their plasticities. NCN_grant 2021/43/B/NZ4/01675