TCF7L2 is a high-confidence risk gene for neurodevelopmental disorders (NDs), but its role in their pathogenesis is unknown. It is highly expressed in the thalamus - candidate structure for NDs pathogenesis - regulating its electrophysiological maturation. To understand the role of thalamus-expressed Tcf7l2 in signal processing in thalamocortical circuits, we investigated consequences of its deficiency in the somatosensory circuit: first- and higher-order thalamic nuclei (VPM and POM) and the barrel cortex.Tcf7l2 postnatal thalamic knockout mice were used to assess signal gating mechanism in vivo (with prepulse inhibition paradigm and Neuropixels recordings). Moreover, we measured spontaneous miniature postsynaptic currents in vitro.Male knockout mice showed gating deficits across all considered areas - VPM (t(11) = 2.73, p <0.01); cortical layer 4 (t(17) = 2.22, p <0.05); 5 (t(22) = 2.17, p <0.05); 6 (U =23, p <0.0001) and POM (t(57) - 2.63, p <0.01). In females, minor differences were observed in VPM (t(30) = 2.13, p <0.05) and cortical layer 5 (t(25) = 2.31, p <0.05).Patch-clamp showed that the frequency of mIPSC was greatly decreased in VPM (U = 66, p <0.0001), while neurons of cortical layers 4 (U = 22, p <0.01) and 6 (t(13) = 2.51, p <0.05) showed frequency decrease in mEPSC.TCF7L2 deficiency in thalamic neurons leads to signal processing impairments in thalamocortical circuits. While the deficit in inhibitory activity in the thalamus is congruent with theimpairment of gating, the decrease of excitation in cortical neurons might indicate the presence of compensatory mechanisms.