Anti-NMDA receptor (NMDAR) encephalitis is associated with the presence of autoantibodies against subunit 1 of the NMDA receptor (NR1) resulting in a variety of psychiatric symptoms as well as cognitive and motor impairments. These autoantibodies can arise in adulthood but also during pregnancy where they have been shown to affect the developing foetal brain and are implicated in neurodevelopmental disorders including autism and learning disabilities. Binding of these autoantibodies causes internalization of surface NMDAR leading to their reduced expression and disrupted signalling. To what extent specific developing brain circuits are sensitive to NR1 NMDAR antibodies is largely unknown. The aim of our study is to explore how brief and early exposure to patient-specific antibodies against NR1 affects neuronal circuits in the developing mouse striatum, a brain region involved in motor and cognitive control. We examined how in utero intraventricular injections of NR1 or control immunoglobulins (IgGs) at embryonic day (E)14.5 affect the developing striatum during both pre- and postnatal stages through patch-clamp recordings, immunohistochemistry, and behavioural testing. We find high levels of NR1 expression in the primordial striatum/lateral ganglionic eminence at prenatal stages as well as changes in the proliferation and migration of embryonic progenitors after exposure to NR1 antibodies. At early postnatal stages we observe smaller striatal volume and altered corticostriatal synaptic connections and intrinsic properties of striatal neurons, which is also reflected in altered mouse behaviour. In conclusion, our findings show that in utero exposure of patient-derived NR1-IgGs can result in prolonged cellular and circuit changes in striatum.