Mammalian cortical function relies on the intricate interplay between inhibitory interneurons and excitatory pyramidal cells. Parvalbumin-expressing (PV) interneurons represent the most abundant subclass of cortical interneurons and are essential for the gating of excitatory cells activity. The transcriptional co-activator PGC1a, encoded by the 'Ppargc1a' gene (Peroxisome proliferator activated receptor-gamma co-activator 1-alpha), is a master regulator of mitochondrial biogenesis and has been suggested to be important for the proper functioning of PV interneurons. However, the precise pattern of expression of 'Ppargc1a' and its role in the maturation of PV interneurons during development are yet to be established. Here, we investigate whether the maturation of cortical PV interneurons is controlled by the activity- dependent modulation of 'Ppargc1a' expression levels. Using in situ hybridization and immunohistochemistry throughout mouse postnatal development, we first show that 'Ppargc1a' is expressed in selected classes of cortical interneurons. This includes prospective PV interneurons, in which 'Ppargc1a' is enriched before the onset of their maturation. There, PGC1a seems to be required for the expression of a PV-specific genetic programme that is altered upon conditional deletion of 'Ppargc1a' in interneurons derived from the medial ganglionic eminence. By interfering with the formation of excitatory synapses contacting PV interneurons, we find that 'Ppargc1a' expression during development seems to depend on the excitatory inputs received by these cells. Finally, using chemogenetic tools, we also uncover a novel mechanism by which abnormal network hyperactivation inhibits 'Ppargc1a' expression and PV interneuron maturation. Overall, our results suggest that PGC1a functions as a cell-intrinsic molecular hub translating extrinsic cues into transcriptional programmes to drive the terminal differentiation of PV interneurons.