How the brain effectively switches between and maintains global states, such as sleep and wakefulness, is not yet understood. We used brainwide functional imaging at single-cell resolution to show that during the developmental stage of lethargus, the brain is predisposed to global quiescence, characterized by systemic down-regulation of neuronal activity. Only a few specific neurons are exempt from this effect. In the absence of external arousing cues, this quiescent brain state arises by the convergence of neuronal activities toward a fixed-point attractor embedded in an otherwise dynamic neural state space. We observed efficient spontaneous and sensory-evoked exits from quiescence. Our data support the hypothesis that during global states such as sleep, neuronal networks are drawn to a baseline mode and can be effectively reactivated by signaling from arousing circuits.
Modern recording techniques enable large-scale measurements of neural activity in a variety of model organisms. The dynamics of neural activity shed light on how organisms process sensory information and generate motor behavior. Here, we study these dynamics using optical recordings of neural activity in the nematode C. elegans. To understand these data, we develop state space models that decompose neural time-series into segments with simple, linear dynamics. We incorporate these models into a hierarchical framework that combines partial recordings from many worms to learn shared structure, while still allowing for individual variability. This framework reveals latent states of population neural activity, along with the discrete behavioral states that govern dynamics in this state space. We find stochastic transition patterns between discrete states and see that transition probabilities are determined by both current brain activity and sensory cues.Our methods automatically recover transition times that closely match manual labels of different behaviors, such as forward crawling, reversals, and turns. Finally, the resulting model can simulate neural data, faithfully capturing salient patterns of whole brain dynamics seen in real data. Tonic signaling from O 2 sensors sets neural circuit activity and behavioral state. Nature neuroscience, 15(4):581, 2012. M. Chalfie, J. E. Sulston, J. G. White, E. Southgate, J. N. Thomson, and S. Brenner. The neural circuit for touch sensitivity in Caenorhabditis elegans. Journal of Neuroscience, 5(4):956-964, 1985. C.-B. Chang and M. Athans. State estimation for discrete systems with switching parameters. IEEE Transactions on Aerospace and Electronic Systems, AES-14(3):418-425, 1978. Z. Chen, S. N. Gomperts, J. Yamamoto, and M. A. Wilson. Neural representation of spatial topology in the rodent hippocampus. Neural Computation, 26(1):1-39, 2014. Monte Carlo sampling for tuning-curve analysis. J. Neurophysiol., 103(1):591-602, Jan. 2010. J. P. Cunningham and M. B. Yu. Dimensionality reduction for large-scale neural recordings. Nature neuroscience, 17(11):1500, 2014. P. Dayan and L. F. Abbott. Theoretical neuroscience: computational and mathematical modeling of neural systems. MIT press, 2001. A. P. Dempster, N. M. Laird, and D. B. Rubin. Maximum likelihood from incomplete data via the EM algorithm.
Axonal degeneration is a characteristic feature of neurodegenerative disease and nerve injury. Here, we characterize axonal degeneration in Caenorhabditis elegans neurons following laser-induced axotomy. We show that this process proceeds independently of the WLDS and Nmnat pathway, and requires the axonal clearance machinery that includes the conserved transmembrane receptor CED-1/Draper, the adaptor protein CED-6, the guanine nucleotide exchange factor complex Crk/Mbc/dCed-12 (CED-2/CED-5/CED-12) and the small GTPase Rac1 (CED-10). We demonstrate that CED-1 and CED-6 function non-cell-autonomously in the surrounding hypodermis, which we show acts as the engulfing tissue for the severed axon. Moreover, we establish a function in this process for CED-7, an ATP-binding cassette (ABC) transporter, and NRF-5, a lipid-binding protein, both associated with release of lipid-vesicles during apoptotic cell clearance. Thus, our results reveal the existence of a WLDS /Nmnat-independent axonal degeneration pathway, conservation of the axonal clearance machinery, and a function for CED-7 and NRF-5 in this process.
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