Dr. Fuller's research focuses on brain substrates of behavioral state control, including the temporal organization of behavioral state imparted by the hypothalamic circadian clock. This work spans a discontinuous continuum from coma (irreversible absence of wakeful consciousness), to sleep (reversible absence of wakeful consciousness), to the fullest expression of wakeful consciousness (complete neurobehavioral and electroencephalographic (EEG) arousal). In undertaking this work, the Fuller lab has sought to identify and characterize the key circuits, nodes, cell populations and transmitters that are necessary for normal levels and manifestations of neurobehavioral and EEG phenomenon during

1. wakefulness/cortical arousal, and
2. sleep.

Damage to discrete subcortical cell populations can reduce conscious awareness or even produce coma after stroke or brain injury, and work in the Fuller lab seeks to promote recovery by manipulating these neurons, and/or their postsynaptic targets. In addition, a more detailed understanding of the brain substrates that initiate, organize and maintain sleep will not only provide a better understanding of how sleep contributes to normal brain function, but may also inform how disrupted sleep could be improved in a wide range of neurologic, neurodegenerative and neuropsychiatric conditions, e.g., Alzheimer's disease, TBI, PTSD. 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 Ca+2-based imaging and optetrode/LFP recordings, optogenetics, chemogenetics, single neuron and single nuclei transcriptomics, and cell-specific mapping techniques.