The role of thalamus in sleep, wake and cognitive processing

Thalamic stroke occurs in a deep part of the brain caused by either an ischemic event (artery clot) or by hemorrhagic rupture or leakage of a blood vessel. Though the thalamus represents a small area of the brain, it controls a big part of how our bodies function and respond to our environment. The thalamus sends has dense connections to all the parts of the brain and receives information from all parts of the brain. Thus, thalamic strokes result wide range of events, including speech, memory, balance, motivation impairments, and sensations of physical touch and pain. Recovery is more challenging for these types of strokes because there are many more areas of the brain involved.

Here, we propose to combine a photo-thrombotic stroke model that allows the production of minor and localized strokes in order to dissect the anatomical and functional changes that may arise by lesion of specific areas of the thalamus (comparing bilateral and unilateral lesions that result in different recovery prognosis in humans). We use EEG and local filed potentials (LFP) to characterize changes in sleep oscillations and architecture, and will use an optogenetic approach to modulate thalamic target areas of the distinct circuitries to recover behavioral deficits (e.g. pain, cognitive and sensory processing) that are associated with the mini-stroke lesions. Additionally, local manipulation of distinct mouse thalamic circuitries will closely reflect sleep disturbances, and behavioral deficits similar to the ones observed in humans. This multidimensional approach will allow for establishing necessary links between structure and function from acute to the chronic phases of the stroke lesions and consequences.