{{item.date}}
{{subItem.title}}
{{subItem.subtitle}}




美国斯坦福大学 Stanford University, United States
教授 Professor
Dr. de Lecea obtained his PhD degree from the University of Barcelona and moved to The Scripps Research Institute in 1992. He progressed through the ranks at Scripps and he moved to Stanford University in 2006, where he remains as a tenured Professor in the Department of Psychiatry and Behavioral Sciences. Dr. de Lecea’s work is based on the discovery of several neuropeptides with key roles in brain states. In particular, he first identified the Hypocretins (also known as orexins), two neuropeptides that have served as a “Rosetta stone” to identify the language of sleep/wake transitions. His laboratory was also first to implement optogenetic methods in vivo. Dr. de Lecea has served on multiple national and international committees and editorial boards. He is also recipient of multiple awards including Fullbright Senior Scholar, Peking University Fellow, NARSAD Distinguished Investigator, Sleep Research Society Outstanding Research Achievement Award, ACNP Integrative Neuroscience Award.
报告题目:
Sleep/wake control across lifespan
报告摘要:
The arousal construct underlies a spectrum of behaviors that include sleep, exploration, feeding, sexual activity and adaptive stress. Pathological arousal conditions include stress, anxiety disorders, and addiction. In the past few years we have used optogenetics to interrogate neuronal circuits underlying transitions between arousal states. Here I will present causal evidence of a critical period during adolescence in which disruption of sleep/wake cycles associated with increased dopaminergic tone results in deficits in social interactions in adult mice. I will also present a new mechanism underlying sleep fragmentation during aging. Hcrt neurons are hyperexcitable in aged mice. We identify a potassium conductance known as the M-current, as a critical player in maintaining excitability of Hcrt neurons. Genetic disruption of KCNQ channels in Hcrt neurons of young animals results in sleep fragmentation. In contrast, treatment of aged animals with a KCNQ channel opener restores sleep/wake architecture. These data point to multiple circuits modulating sleep integrity across lifespan. Finally, I will show how we are using ultrasound neuromodulation to harness the neuronal circuitry governing sleep and wakefulness.
{{subItem.subtitle}}
Dr. de Lecea obtained his PhD degree from the University of Barcelona and moved to The Scripps Research Institute in 1992. He progressed through the ranks at Scripps and he moved to Stanford University in 2006, where he remains as a tenured Professor in the Department of Psychiatry and Behavioral Sciences. Dr. de Lecea’s work is based on the discovery of several neuropeptides with key roles in brain states. In particular, he first identified the Hypocretins (also known as orexins), two neuropeptides that have served as a “Rosetta stone” to identify the language of sleep/wake transitions. His laboratory was also first to implement optogenetic methods in vivo. Dr. de Lecea has served on multiple national and international committees and editorial boards. He is also recipient of multiple awards including Fullbright Senior Scholar, Peking University Fellow, NARSAD Distinguished Investigator, Sleep Research Society Outstanding Research Achievement Award, ACNP Integrative Neuroscience Award.
报告题目:
Sleep/wake control across lifespan
报告摘要:
The arousal construct underlies a spectrum of behaviors that include sleep, exploration, feeding, sexual activity and adaptive stress. Pathological arousal conditions include stress, anxiety disorders, and addiction. In the past few years we have used optogenetics to interrogate neuronal circuits underlying transitions between arousal states. Here I will present causal evidence of a critical period during adolescence in which disruption of sleep/wake cycles associated with increased dopaminergic tone results in deficits in social interactions in adult mice. I will also present a new mechanism underlying sleep fragmentation during aging. Hcrt neurons are hyperexcitable in aged mice. We identify a potassium conductance known as the M-current, as a critical player in maintaining excitability of Hcrt neurons. Genetic disruption of KCNQ channels in Hcrt neurons of young animals results in sleep fragmentation. In contrast, treatment of aged animals with a KCNQ channel opener restores sleep/wake architecture. These data point to multiple circuits modulating sleep integrity across lifespan. Finally, I will show how we are using ultrasound neuromodulation to harness the neuronal circuitry governing sleep and wakefulness.