While for many years cancer research has mainly focused on targeting tumoral cells, recent studies have confirmed that the tumor microenvironment (TME) plays a major role in controlling glioma growth. Indeed, several studies have highlighted that the synaptic activity of pyramidal, glutamatergic neurons potently drives Glioblastoma (GB) proliferation. However, the role played by other neuronal cell types is still poorly understood. Here, we wanted to dissect the role of peritumoral interneurons in GB development. Taking advantage of chemogenetics, we modulated the activity of parvalbumin (PV)-interneurons during GB growth in order to elucidate whether the activity of those cells might affect tumoral growth in the murine motor cortex. We found that PV-interneurons activation exert no effect on the median survival of CNO-treated glioma bearing mice with respect to the control mice (32 vs 29 days). Interesting, Magnetic Resonance Imaging (MRI) showed a very significative reduction in the tumor volume at 28 days after glioma induction in CNO-treated glioma bearing mice (p=0,004). These data suggest that the inhibitory circuitry in the tumor-adjacent zone could delay GB growth, protecting peritumoral tissue from GB proliferation. Understanding the complex relationship between GB and tumor microenvironment could help in developing effective therapeutic approaches aimed at ameliorating patients’ quality of life and survival.