<EM>IN VIVO </EM>CHARACTERIZATION OF PV AND SST INTERNEURON DEVELOPMENT IN THE PRIMARY VISUAL CORTEX: IMPLICATIONS FOR NEURODEVELOPMENTAL DISORDERS

Developmental dysregulation of GABAergic interneurons, particularly parvalbumin (PV-INs) and somatostatin (SST-INs) interneurons, has been implicated in neurodevelopmental disorders such as autism and schizophrenia. Postnatal interactions with local glutamatergic circuits are critical for interneuron maturation, yet the cell-type-specific mechanisms governing this process in vivo remain poorly understood. We longitudinally characterized the functional maturation of PV-INS and SST-INS in layer 2/3 of mouse primary visual cortex using two-photon calcium imaging during visually evoked activity, spanning early post–eye-opening stages through adulthood. Recordings were obtained from PV-Cre and SST-Cre mice expressing GCaMP8s. To probe the role of glutamatergic signaling, we examined mice with conditional deletion of GluN1, given the strong association between NMDAR dysfunction and neurodevelopmental disorders. In adult animals, both PV- and SST-INs were broadly tuned for orientation. However, SST-INs exhibited stronger contrast modulation, slower response dynamics, and prominent contrast-dependent sharpening of orientation tuning, whereas PV-INs showed faster, more weakly modulated responses. Developmentally, SST-IN orientation tuning was already present at P15–19, yet contrast sensitivity emerged slowly over subsequent postnatal stages. In contrast, preliminary data suggest that PV-INs were initially more sharply tuned early after eye opening. Conditional GluN1 deletion had minimal effects on adult PV-IN responses but significantly reduced the magnitude and altered the temporal dynamics of visually evoked activity in SST-INs, with preliminary analyses indicating a marked disruption of their developmental trajectory. Together, these findings reveal prolonged, cell-type-specific maturation of inhibitory circuits in visual cortex and identify SST-IN functional development as a slow, NMDAR-dependent process.