One of the mechanisms by which the experience-dependent reorganization of neural circuitry can occur is through changes in synaptic strength. Many excitatory synapses in the mammalian brain exhibit LTP (long-term potentiation) or LTD (long-term depression), two cellular mechanisms of synaptic plasticity. However, LTP and LTD have been reported much more rarely at fast inhibitory GABAA receptor synapses. Our recent study suggests that in vivo morphine initiates a long-lasting alteration of GABAergic synapses in the ventral tegmental area (VTA) by blocking the mechanisms required for LTP of GABAergic synapses. Here we put this work into the context of other examples of synaptic plasticity at GABAergic synapses.