Down syndrome (DS) results from chromosome 21 trisomy, causing cognitive and developmental challenges often accompanied by hearing deficits. Studies on humans using EEG and MEG have identified prolonged latencies in sound-evoked responses in DS. However, the origin and characteristics of these deficits remain unclear. This study investigates auditory processing in a DS rat model to determine whether sensory deficits arise from early processing areas, such as the auditory thalamus and primary auditory cortex (A1), or higher-level cognitive alterations. We conducted neural activity recordings, using 384 channel Neuropixel probes, in A1 and the auditory thalamus of anesthetized DS and wild-type (WT) rats aged between 4 and 7 months. Based on preliminary data from 8 animals, we identified differences between the two groups in both thalamus and cortex. Thalamic neurons in WT animals were more sensitive (by up to 5 dB) than neurons recorded in DS animals. In A1, we found a larger proportion of units with delayed responses (50ms or greater) in DS compared to WT. Ongoing behavioral studies investigating auditory stimulus detection performance so far suggest that both DS and WT rats can detect high amplitude auditory targets. Further tests with stimulus target amplitude close to threshold will reveal if apparent deficits in sensory neural processing impact behavioral performance. Our results suggest that at neural circuit level DS has a moderate impact on auditory processing. These sensory pathway deficits provide a precise avenue for quantifying neural dysfunction related to DS, and for assessing utility of therapeutic interventions such as neuromodulation.