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Sensory processing across sleep, anesthesia, and lapses: The role of reduced noradrenaline signaling - Yuval Nir

Stanford Neurosciences Institute, Yuval Nir
November 9, 2018 - 10:00am
Munzer Auditorium

Yuval Nir

 

Sagol School of Neuroscience
Department of Physiology and Pharmacology
Sackler School of Medicine
Tel Aviv University, Israel

Abstract

Sensory disconnection" – when the same sensory stimulus does not reliably affect behavior or subjective experience - is a defining feature of sleep, and similar processes may occur during light anesthesia or during cognitive lapses. What are the changes in brain activity that mediate sensory disconnection? In a series of studies in humans and rodents, we investigate how "disconnected" states affect sensory processing. The first set of studies reveals differences in neuronal responses to identical sensory stimuli across states.  In humans, cognitive lapses after sleep deprivation involve attenuated and delayed single-neuron responses in MTL co-occurring with local slow/theta waves.  In the auditory domain, in both rodents and humans responses in sleep and light anesthesia are preserved up to A1, challenging the classic "thalamic gating" notion. Instead, robust attenuation occurs later in high-level cortical regions. In addition, sleep affects more strongly responses that require integration over long time intervals, and responses to high-frequency content. The second set of studies investigates the underlying mechanisms, testing the potential role of locus coeruleus-noradrenaline (LC-NE) neuromodulation. In rats, we test how NE signaling affects the probability of sound-evoked awakening from sleep. We establish selective in-vivo LC optogenetics by showing effects on spiking activity, evoked sleep-wake transitions, and pupil dilation. Auditory stimulation on a background of weak LC-NE modulation synergistically increases the probability of awakenings beyond independent effects of sound and laser alone, supporting a role for LC-NE activity in mediating sensory responses. We also tested the effects of NE levels on perception and sensory-evoked activity (EEG, fMRI) in awake humans. Pharmacologically manipulating NE levels in double-blind placebo-controlled experiments, we find that NE modulates visual perception and boosts late visual responses, suggesting that NE is a key factor causally linking sensory awareness to external world events

Event Sponsor: 
Dr. de Lecea (Professor of Psychiatry and Behavioral Sciences)
Contact Email: 
Ayesha Abid <aabid@stanford.edu>