During development, medial olivocochlear (MOC) neurons transiently innervate inner hair cells (IHCs). After hearing onset (P12–14), they establish permanent synapses onto outer hair cells (OHCs), integrating feedback from peripheral and central circuits. We recently showed that MOC terminals co-release acetylcholine (ACh) and GABA: ACh activates postsynaptic α9α10 receptors, whereas GABA engages presynaptic GABAB receptors that reduce ACh release. Here, we examined how GABAB -mediated inhibition shapes short-term plasticity at MOC–IHC and MOC–OHC synapses. In acutely isolated organs of Corti (P9–P15), IPSCs were recorded from hair cells during electrical stimulation of MOC fibers. In IHCs, 10 pulses at 50 Hz produced synaptic depression (P10/P1 = 0.54). Baclofen, a GABAB agonist, abolished depression (P10/P1 = 1), whereas the antagonist CGP35348 increased depression even at 10 Hz. At MOC–OHC synapses, blocking GABAB reduced facilitation during 50 Hz stimulation (P10/P1control = 1.69 vs. P10/P1antag. = 1.09). These results suggest that presynaptic GABAB receptors minimize depression at MOC–IHC synapses and promote facilitation at MOC–OHC synapses, supporting sustained transmission during high-frequency activity.