To study homeostatic feedback regulation, we performed two-electrode voltage clamp (TEVC) recordings at NMJs of Drosophila larvae lacking the glutamate receptor subunit IIA (GluRIIA) and controls. In these mutants, amplitudes of miniature excitatory postsynaptic currents (mEPSCs) were reduced compared to controls (GluRIIA mutant: 0.55 nA ±0.02, n = 7; control: 1.21 nA ±0.09, n = 5; Student's t-test: P < 0.001), but nerve-evoked EPSC amplitudes were not significantly altered (mutant: 39.2 nA ±3.6, n = 7; control: 41.8 nA ±4.6, n =9; P = 0.7), indicating an enlarged quantal content in the mutants. To analyse the mechanisms of this presynaptic compensation, short-term plasticity during high-frequency stimulation (100 stimuli at 60Hz) was investigated. Synaptic depression was slightly more pronounced in GluRIIA mutants compared to controls. However, the differences in short-term plasticity were small, indicating only subtle changes in release probability (p_r ), which probably cannot account for the large increase in quantal content. Rather, these data suggest that the observed synaptic phenotype is due to a larger number of readily releasable vesicles (N). Consistently, in first experiments using fluctuation analysis, N was elevated to 490 ±190 (n = 2) in GluRIIA mutants compared to 350 ±70 (n = 8) in control larvae, while p_r was not increased. Taken together, our results suggest a compensatory increase in the number of readily releasable vesicles at NMJs of postsynaptic GluRIIA mutant Drosophila larvae.