Fast synaptic inhibition is largely mediated by GABAA receptors (GABAARs), ligand-gated chloride channels that play an essential role in the control of cell and network activity in the brain. The delivery, number and stability of GABAARs at inhibitory synapses play a key role in the dynamic regulation of inhibitory synaptic efficacy and plasticity. The pathways essential for the fine-tuning of synaptic inhibition have also emerged as key sites of vulnerability during pathological changes in cell excitability in disease states. Here I will present some of our latest findings on the role played by receptor interacting proteins and post-translational modifications in modulating GABAAR membrane dynamics and synaptic delivery and hence the strength of inhibitory neurotransmission under normal conditions and in pathology.