Sleep deficits are often prodromal to the onset of psychiatric diseases. Such disorders, for example schizophrenia, autism spectrum disorder or attention deficit hyperactivity disorder, are strongly linked to the 22q11.2 microdeletion (22qdel). Carriers of 22qdel exhibit reduced sleep spindle formation, which correlates to decreased memory performance and disease severity. Two neurological cell populations, the noradrenergic (NA) neurons in the locus coeruleus (LC) and the parvalbumin (PV)-positive cortical interneurons are involved in the regulation of sleep spindles. However, the interplay of NA-dependent sleep microstructures and PV interneurons with sleep spindle generation remains unknown. We aim to uncover the neural basis of sleep and memory deficits in psychiatric disorders, hypothesizing that sleep disturbances are causative rather than mere consequences of 22qdel. A well-characterized mouse model of 22qdel, the LgDel mice, are implanted with electroencephalogram and electromyography electrodes. Combined with fluorescent biosensors to monitor NA activity in the thalamus and PV neuron activity in the prefrontal cortex, fiber photometry is used for the functional assessment during sleep in freely moving animals. Preliminary results show an overall alteration of LgDel’s sleep composition and indicate fewer microarousals, suggesting downregulation of LC activity which allows for upregulated PV interneuron signaling. Additionally, changes in social and memory-based behaviour tasks can be observed. This study provides a unique perspective on the interaction between NA-dependent sleep microstructures and PV interneurons in 22qdel, paving the way for biomarkers and therapeutic interventions for neuropsychiatric symptoms associated with sleep dysfunction.