Dr. Satvinder Kaur is having 20 years of experience with acquisition and analysis of various physiological recordings and behavioral assays. With her broad background of accomplishments in sleep physiology/ neurobiology, she possesses the expertise and training to carry out the work outlined in this current proposal. Her research delves into understanding the neural circuitries that regulate sleep (rapid eye movement-REM and non-rapid eye movement-NREM), sleep homeostasis after sleep loss/ deprivation, spontaneous and CO2- induced wakefulness (as seen in apneas). During her scientific research career, she demonstrated continued productivity as evident through her scientific publications, authorships on three-book chapters and numerous scientific abstracts.

The investigative approaches for studying these neural pathways included long term recordings and analysis of the behavioral parameters such as EEG/ EMG, EKG, body temperature. She employed the chronic telemetry as well as the tethering cables for more stable and noise free recordings in freely moving rodents. In addition, she also employs various specific neurotoxins and viral vector systems in mouse-based experiments to conduct deletions of specific neurons or express specific genes in selective cell populations, and these are injected in the brains via micro-stereotaxic surgical procedures. For analyses of the cell specific neurotoxic and pharmaco-genetic lesions, identifying the site of delivery and transfection of the different viral vectors, she used the standard immune-histochemical labeling techniques and have conducted analysis of the labeled tissue using bright field, fluorescence and confocal microscopy.

She is currently an Instructor in the Department of Neurology at Beth Israel Deaconess Medical Center and Harvard Medical School. She is working on understanding the underlying mechanisms and the neural circuits that are responsible for the control of arousal during apnea. They have developed a mouse model to study the mechanism of apnea-induced arousals (Kaur et al., 2013). Using the Cre- Lox recombination technology, they could dissect the neuro-circuitry underlying hypercapnia induced arousals, and identified an area in the lateral PB that regulates cortical arousals to CO2. Now, she is using various optogenetic and pharmaco-genetic tools to genetically target the neuro-circuitry and pathways that control arousals during apnea. She recently presented her results at the SLEEP 2015 meeting in Seattle, where she used optogenetics to selectively target the acute inhibition of the PBel-CGRP neurons (Kaur et al., 2015). The results from this study greatly complement the specific aims outlined in the present proposal, and extend the present acute studies to understanding the chronic effects of apneas on sleep and metabolism.

Neural circuitries that regulate sleep (rapid eye movement-REM and non-rapid eye movement-NREM); Sleep homeostasis after sleep loss/ deprivation; Spontaneous and CO2- induced wakefulness (as seen in apneas).