Numerous brain pathologies are characterized by an imbalance between excitatory and inhibitory actions in brain microcircuits. The loss or loss of function of parvalbumin-positive interneurons (PV+), an interneurons subtype, is accompanied by network disturbance and cognitive dysfunction in many neuro-psychiatric diseases. Platelet-activating factor acetylhydrolase 1B subunit alpha (known as Lis1) is a regulator of dynein mediated motility, mitosis nuclear positioning and microtubule organization. Lis1 gene mutation has been associated with lissencephaly in humans and defects in neural migration or epilepsy. We have generated an animal model, in which Lis1 gene is deleted in PV+ interneurons specifically, to analyze the role of Lis1 in interneurons. We focused on anatomical consequences of Lis1 silencing. We have studied the number of PV+ interneurons in the cingulate cortex (cingulate anterior and retrosplenial cortices) and the possible alteration in their activity, using cFos as an activity marker by three-dimensional immunohistochemistry (iDSICO protocol) to explore the whole brain postnatally. Our results show a PV+ interneurons reduction in the cingulate cortex (48%) of mutant mice compared to controls with a reduction in cortical layers II/III, V and VI (51%, 47%, and 35%). This result suggests an alteration of the interneuron migration, maturation and/or cell apoptosis. Moreover, we also observed an increase of cFos+/PV- cells at different cerebral regions, including cingulate cortex and specific hypothalamic nuclei. More experiments will be necessary to understand the underlying mechanisms of this effects, as well as to evaluate the functional consequences derived from these alterations. Research supported by MCIN grant-PID2020-118171RB-I00, GVA-Prometeo Grant-CIPROM/2021/018.