Patrick Fuller, PhD

Dr. Fuller's research focuses on the brain substrates that control behavioral states, including the temporal organization of behavioral states regulated by the hypothalamic circadian clock. This research spans a discontinuous continuum, ranging from coma (irreversible absence of wakeful consciousness) to sleep (reversible absence of wakeful consciousness) to the fullest expression of wakeful consciousness, which involves complete neurobehavioral and electroencephalographic (EEG) arousal.

In pursuing this research, the Fuller lab aims to identify and characterize the key circuits, nodes, cell populations, and transmitters necessary for normal levels and manifestations of neurobehavioral and EEG phenomena during wakefulness/cortical arousal, as well as sleep. Damage to discrete subcortical cell populations can reduce conscious awareness or even lead to coma following stroke or brain injury. Work in the Fuller lab focuses on promoting recovery by manipulating these neurons and their postsynaptic targets.

Moreover, gaining a more detailed understanding of the brain substrates that initiate, organize, and maintain sleep is not only essential for understanding how sleep contributes to normal brain function but can also inform strategies to improve disrupted sleep in a wide range of neurologic, neurodegenerative, and neuropsychiatric conditions, such as Alzheimer's disease, traumatic brain injury (TBI), and post-traumatic stress disorder (PTSD).

The Fuller lab is also interested in understanding how the hypothalamic suprachiasmatic clock (SCN) regulates the temporal architecture of the sleep-wake cycle and the cellular mechanisms by which the SCN clock appears to promote and maintain normal levels of arousal at the end of the biological day

To address these challenges, the Fuller lab has employed and developed a wide range of methodologies, including morphological methods, genetic engineering techniques in mice and rats, brain slice electrophysiology, in vivo single-cell and population Ca2+-based imaging, optetrode/LFP recordings, optogenetics, chemogenetics, single neuron and single nuclei transcriptomics, and cell-specific mapping techniques.

Up to this point, the work in the Fuller lab has resulted in numerous papers describing previously unrecognized cell groups, transmitters, and circuits necessary for normal levels of sleep and wakefulness. From a translational perspective, the findings from the Fuller lab have suggested new cellular targets for increasing forebrain activation in dementia and the minimally conscious state, as well as for treating sleep disorders, ranging from primary insomnia to hyperarousal in PTSD and idiopathic hypersomnia.


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Christelle Anaclet, PhD