Activity-dependent changes in mRNA translation are crucial for sustaining altered synaptic strength during plasticity. Despite this, translational mechanisms of inhibitory synaptic plasticity (iSP), and particularly their role in postsynaptic changes during iSP, are understudied. This dissertation investigates translation during different forms of iSP with a specific focus on inhibitory long-term potentiation (iLTP) and homeostatic upscaling of inhibitory synapses, which are critical for physiological processes such as tuning neuronal excitability, preventing runaway activity, and shaping development of the visual system. The key findings demonstrate that protein synthesis is essential for supporting multiple types of iSP, although its precise role and the mechanisms which govern it can diverge with different plasticity-inducing stimuli. Persistent iLTP requires de novo synthesis of synaptic GABAA receptors (GABAAR) and the inhibitory scaffold gephyrin. Gephyrin synthesis during iLTP is mediated by reduced expression of a microRNA, miR153, which represses its translation under basal conditions. This translational control mechanism is crucial for sustaining iLTP and is driven by an excitationtranscription (E-T) coupling pathway which downregulates miR153 transcription. These signals also reduce transcription of miR376c, which controls synthesis of synaptic GABAAR subunits. Thus, we find that activity can leverage a network of miRNAs to modulate expression of multiple genes involved in GABAergic signaling in order to shape synaptic strength long-term. During homeostatic upscaling of synaptic inhibition, increased clustering at GABAergic synapses begins to emerge within a few hours of elevated activity. These changes require translation, but do not involve de novo synthesis of GABAAR/GPHN, as we observed for persistent iLTP. These results demonstrate that translation is essential for sustaining postsynaptic mechanisms of iSP. However, our findings also allude to the diverse roles that translation can play in these processes and indicate the complexity which underlies the precise control of synaptic inhibition in response to neural activity. Overall, this work contributes to our understanding of activity-dependent changes in gene expression during iSP and provides insight into the mechanisms which control neuronal excitability and firing to support cognitive function.