Shank3 is a postsynaptic cytoskeletal protein that acts as an intracellular scaffold supporting various subsequent synaptic components. Its deficiency is associated with significant changes in the morphology and electrophysiological properties of dopaminergic neurons and the expression of various synaptic proteins affecting normal brain development primarily during the early stages. These disruptions in neuronal circuits lead to changes in social interactions, communication skills, and behavioral patterns, commonly observed in neurodevelopmental disorders like autism. To better understand these complex neurobiological mechanisms, we aimed to examine the synaptic activity of neurons in the striatum brain region of both wild-type mice and Shank3-deficient mice, known for exhibiting autism-like symptomatology. We performed recordings of glutamatergic and GABAergic postsynaptic currents in the primary culture of striatal neurons at 10 – 12 days in vitro. The electrophysiological recordings of spontaneous postsynaptic currents were measured as continuous recordings of postsynaptic current in the whole-cell voltage clamp configuration of the patch clamp method. Our functional analysis of neuronal synaptic activity revealed significant enhancements in the spontaneous postsynaptic activity of striatal neurons derived from Shank3-deficient mice compared to wild-type neurons. Specifically, the average frequency of excitatory and inhibitory postsynaptic currents was notably increased in Shank3-/- neurons compared to wild-type neurons. Additionally, the median amplitude of events was higher in Shank3-/- neurons than wild-type neurons. These findings suggest that the absence of Shank3, associated with autism-like symptoms in the model, disrupts the function of dopaminergic neurons, potentially contributing to the disorder's neurobiological mechanisms. Supported by VEGA 2/0073/22 and APVV-21-0189.