Experiences during wakefulness are replayed during sleep to consolidate the relevant information. At the circuit level, this process is thought to be reflected by the synchronised cortical activity during non-rapid eye movement (NREM) sleep. This cortical synchronisation is described by slow wave activity (0.5 - 4Hz) and the emergence of spindles (10 - 16 Hz). Slow waves and spindles can be recorded locally in one cortical area or globally throughout the cortex. They are often temporally associated with hippocampal ripples (80 - 250 Hz). Our understanding of how local and global sleep oscillations are shaped by various experiences and learning is incomplete, as the majority of the studies examine single modalities with a focus in the prefrontal cortex (PFC). Therefore, this thesis aims to compare the sleep oscillations in PFC and somatosensory cortex (S1) in baseline and upon experiences.

I conducted three sets of experiments. First, I recorded local field potential during baseline sleep in PFC and S1. In agreement with previous reports, I showed that PFC spindles preferentially followed slow waves, while S1 spindles were similarly probable to occur before and after slow waves. In hippocampus, ripples preferentially occurred outside slow waves in PFC, while this observation was weaker in S1. Next, I investigated how experiences shaped sleep oscillations and their temporal associations in PFC and S1 by conducting a PFC dependent appetitive Y-maze and a S1 dependent object exploration task. Task performance enhanced slow wave activity and sigma activity in both cortices, while learning of Y-maze was predicted by a closer temporal association between slow waves and spindles in PFC. In contrast, my preliminary results on the object exploration task suggested that temporal association of oscillations was modified in S1 but not in PFC. Last, I attempted to characterise the mechanism of brain oscillation coordination. Acting as a communication hub between PFC and hippocampus, midline thalamus has the potential of synchronising neocortical oscillations and hippocampal ripples. Using optogenetic tools, I performed a sustained inhibition of midline thalamus and observed an increased peak frequency of spindles in PFC and enhanced sigma oscillations in S1, while temporal association of oscillatory events was differentially modulated in PFC and S1.

My findings indicated that during baseline sleep, the sleep oscillations in PFC and S1 exhibited distinct temporal association with each other. The change in the temporal association of oscillations was confined to the previously engaged cortex during task performance. Additionally, the midline thalamic activity contributed differently to the oscillations in these cortical areas. Together, these results highlighted a different temporal association of oscillatory events in S1 to what has been reported in PFC, with stronger responsiveness to recent sensory experience. Future experiments could be conducted to manipulate oscillatory strengths and temporal association between oscillatory events to establish the causal relationship.