Synaptic plasticity is triggered by different patterns of network activity. Here, we investigated how long-term potentiation (LTP) in CA3-CA1 synapses induced by different stimulation patterns is affected by tonic GABAA conductances in rat hippocampal slices. Spike-timing-dependent (st) LTP was induced by pairing Schaffer collateral stimulation with antidromic stimulation of CA1 pyramidal neurons. Theta-burst-induced (tb) LTP was induced by theta-burst stimulation of Schaffer collaterals. We mimicked increased tonic GABAA conductance by bath application of 30 µM GABA. Surprisingly, tonic GABAA conductance selectively suppressed tbLTP but not stLTP. We combined whole-cell patch-clamp electrophysiology, two-photon Ca2+ imaging, glutamate uncaging, and mathematical modeling to dissect the mechanisms underlying these differential effects of tonic GABAA conductance. We found that Ca2+ transients during pairing of an action potential (AP) with an EPSP were less sensitive to tonic GABAA conductance-induced shunting inhibition than Ca2+ transients induced by EPSP burst. Our results may explain how different forms of memory are affected by increasing tonic GABAA conductances under physiological or pathological conditions, as well as under the influence of substances that target extrasynaptic GABAA receptors (e.g., neurosteroids, sedatives, antiepileptic drugs, and alcohol).