Yaniv Sela

Abstract About half of the neurons in the parabrachial nucleus (PB) that are activated by CO2 are located in the external lateral (el) subnucleus, express calcitonin gene-related peptide (CGRP), and cause forebrain arousal. We report here, in male mice, that most of the remaining CO2-responsive neurons in the adjacent central lateral (PBcl) and Kölliker-Fuse (KF) PB subnuclei express the transcription factor FoxP2 and many of these neurons project to respiratory sites in the medulla.

Highlights • Neuronal DNA damage triggers sleep • Sleep increases DNA repair and reduces cellular homeostatic pressure • Activity of the DNA damage detector Parp1 increases with sleep deprivation • Parp1 activity promotes sleep, chromosome dynamics, and DNA repair Summary The characteristics of the sleep drivers and the mechanisms through which sleep relieves the cellular homeostatic pressure are unclear.

Research Articles, Systems/Circuits Yaniv Sela, Aaron Joseph Krom, Lottem Bergman, Noa Regev and Yuval Nir Journal of Neuroscience 1 April 2020, 40 (14) 2895-2905; DOI: https://doi.org/10.1523/JNEUROSCI.1186-19.2020 Abstract A fundamental feature of sleep is reduced behavioral responsiveness to external events, but the extent of processing along sensory pathways remains poorly understood.