Autism spectrum disorder (ASD) is a term used to describe a wide variety of neurodevelopmental disorders that share manifestations and symptoms including intellectual disabilities, social impairments, delayed speech development and repetitive behaviors. Different animal models of ASD share similar electrophysiological and morphological aberrations at the neuronal level. In particular, previous studies have shown that the developmental maturation of GABAergic circuitry appears altered leading to an excitation/inhibition imbalance in the adult. During neurotransmission, the polarity of the GABAergic response depends on the intracellular [Cl-] of the postsynaptic neuron which is elevated at birth and decreases during the postnatal development to reach adult values in a process known as “GABA switch”. In our project, the on-cell patch clamping technique allows to measure the GABAergic response without altering the intracellular [Cl-]. By puffing muscimol (selective GABAAR agonist) we detect the polarity of the GABA response and by repeating the experiment in animals of increasing ages we can monitor the progression of the GABA switch. Thanks to this technique we study the delay in temporal onset of the “GABA switch” during postnatal development in different transgenic animal models of autism such as Nlgn3 KO and PTEN. In addition, the DFGABA and spontaneous spiking frequency values are measured through on-cell patch clamping, these measurements are repeated until adulthood to verify if the observed abnormalities persist after the developmental period for GABAergic maturation is closed. The project aims to give insights into how early GABAergic defects could lead to autistic behaviors in the adult.