Traditionally, plasticity was considered to belong mostly to excitatory synapses while inhibitory transmission was assumed to be relatively invariant. However, recent evidences demonstrate several types of inhibitory synaptic plasticity, raising the important question of how GABAergic and glutamatergic synaptic plasticity are coordinated during neuronal activity. Here, we found that non‑Hebbian postsynaptic depolarizations of principal cells induced inhibitory postsynaptic long-term potentiation (iLTP) in hippocampal cultures. Interestingly, the same protocols induced depression at glutamatergic synapses (LTD), thus indicating an anti-homeostatic relation between inhibitory and excitatory synaptic plasticity. Photolysis of caged glutamate or caged GABA revealed that the aforementioned glutamatergic LTD and GABAergic iLTP are expressed postsynaptically. Subsequently, we investigated how synaptic plasticity induced at individual glutamatergic spines affects the strength of neighboring GABAergic synapses. To this end we induced “single spine LTP” by pairing the postsynaptic depolarizations with repetitive glutamate uncaging at individual spines while simultaneously measuring the strength of adjacent dendritic GABAergic synapses by GABA uncaging. Interestingly, we found that, following the delivery of this hebbian-like protocol, GABAergic synapses located within 3 micrometers from a stimulated spine showed depression (iLTD), while further synapses still showed iLTP. This “spread” of heterosynaptic plasticity from spines was dependent on the protease activity of calpain induced by calcium influx through L‑type voltage gated calcium channels. Our findings suggest that both glutamatergic and GABAergic synaptic plasticity are finely coordinated at dendritic level suggesting that the dendritic E/I ratio can be selectively tuned in spatially restricted dendritic sub‑regions.