Behavioral States

Flavell, Steven W.; Raizen, David M.; You, Young-Jai

doi:10.1534/genetics.120.303539

Cited by 60 publications

(50 citation statements)

References 169 publications

(285 reference statements)

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“…To then examine whether HySyn could be used to reconnect specific circuits, we used it to repair a broken neuromodulatory connection. In C. elegans , the serotonergic neuron called NSM regulates a behavioral switch between two states : a high-speed roaming state that occurs in the absence of food, and a low-speed dwelling state that occurs in the presence of food 30 , 31 . NSM is an enteric neuron in the pharynx that senses the presence of bacteria ( C. elegans food) via the use of an acid-sensing ion channel (an ASICs channel) called DEL-7 32 .…”

Section: Resultsmentioning

confidence: 99%

A genetically encoded tool for reconstituting synthetic modulatory neurotransmission and reconnect neural circuits in vivo

et al. 2021

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Chemogenetic and optogenetic tools have transformed the field of neuroscience by facilitating the examination and manipulation of existing circuits. Yet, the field lacks tools that enable rational rewiring of circuits via the creation or modification of synaptic relationships. Here we report the development of HySyn, a system designed to reconnect neural circuits in vivo by reconstituting synthetic modulatory neurotransmission. We demonstrate that genetically targeted expression of the two HySyn components, a Hydra-derived neuropeptide and its receptor, creates de novo neuromodulatory transmission in a mammalian neuronal tissue culture model and functionally rewires a behavioral circuit in vivo in the nematode Caenorhabditis elegans. HySyn can interface with existing optogenetic, chemogenetic and pharmacological approaches to functionally probe synaptic transmission, dissect neuropeptide signaling, or achieve targeted modulation of specific neural circuits and behaviors.

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Section: Resultsmentioning

confidence: 99%

A genetically encoded tool for reconstituting synthetic modulatory neurotransmission and reconnect neural circuits in vivo

et al. 2021

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“…When satiety quiescence was measured using an automated system (Gallagher et al, 2013a), the knockdown of 10 flp genes showed altered satiety quiescence (Figure 1A and Table 1). Previous studies defined several behavioral states based on locomotive activities (Fujiwara et al, 2002;Gray et al, 2005;Ben Arous et al, 2009;Gallagher et al, 2013a;Flavell et al, 2020). Roaming is a state when an animal moves straight in a relatively high speed to explore, dwelling is a state when an animal moves back and forth in a low speed to exploit, and quiescence is a state when an animal is not moving.…”

Section: An Rnai Screen Of 28 Flp Genes Identified Flp-11 In Ris As a Major Regulator Of Satiety Quiescencementioning

confidence: 99%

“…Caenorhabditis elegans, with its powerful genetics and simple nervous system, emerges as an ideal model to study neuromolecular mechanisms underlying sleep. Two types of sleep, developmentally timed sleep (DTS), and stress-induced sleep (SIS), share fundamental aspects of sleep in other animals (Flavell et al, 2020). Additionally, we reported that the C. elegans behavioral state satiety quiescence mimics certain aspects of postprandial sleep in mammals (You et al, 2008).…”

Section: Introductionmentioning

confidence: 96%

Regulation of Satiety Quiescence by Neuropeptide Signaling in Caenorhabditis elegans

et al. 2021

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Sleep and metabolism are interconnected homeostatic states; the sleep cycle can be entrained by the feeding cycle, and perturbation of the sleep often results in dysregulation in metabolism. However, the neuro-molecular mechanism by which metabolism regulates sleep is not fully understood. We investigated how metabolism and feeding regulate sleep using satiety quiescence behavior as a readout in Caenorhabditis elegans, which shares certain key aspects of postprandial sleep in mammals. From an RNA interference-based screen of two neuropeptide families, RFamide-related peptides (FLPs) and insulin-like peptides (INSs), we identified flp-11, known to regulate other types of sleep-like behaviors in C. elegans, as a gene that plays the most significant role in satiety quiescence. A mutation in flp-11 significantly reduces quiescence, whereas over-expression of the gene enhances it. A genetic analysis shows that FLP-11 acts upstream of the cGMP signaling but downstream of the TGFβ pathway, suggesting that TGFβ released from a pair of head sensory neurons (ASI) activates FLP-11 in an interneuron (RIS). Then, cGMP signaling acting in downstream of RIS neurons induces satiety quiescence. Among the 28 INSs genes screened, ins-1, known to play a significant role in starvation-associated behavior working in AIA is inhibitory to satiety quiescence. Our study suggests that specific combinations of neuropeptides are released, and their signals are integrated in order for an animal to gauge its metabolic state and to control satiety quiescence, a feeding-induced sleep-like state in C. elegans.

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“…Organisms such as Drosophila melanogaster have $100,000 neurons and the nematode Caenorhabditis elegans possess $300 neurons. Flies (146) and worms (147) also are open biological systems that display states and features homologous to human states of neurobehavioral arousal.…”

Section: Perspectives Everything Old Is New Againmentioning

confidence: 99%

Prefrontal Cortex Metabolome Is Modified by Opioids, Anesthesia, and Sleep

Lydic

Baghdoyan

2021

Physiology

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Obtundation of wakefulness caused by opioids and loss of wakefulness caused by anesthetics and sleep significantly alter concentrations of molecules comprising the prefrontal cortex (PFC) metabolome. Quantifying state-selective changes in the PFC metabolome is essential for advancing functional metabolomics. Diverse functions of the PFC suggest the PFC metabolome as a potential therapeutic entry point for countermeasures to state-selective autonomic dysfunction.

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Behavioral States

Cited by 60 publications

References 169 publications

A genetically encoded tool for reconstituting synthetic modulatory neurotransmission and reconnect neural circuits in vivo

A genetically encoded tool for reconstituting synthetic modulatory neurotransmission and reconnect neural circuits in vivo

Regulation of Satiety Quiescence by Neuropeptide Signaling in Caenorhabditis elegans

Prefrontal Cortex Metabolome Is Modified by Opioids, Anesthesia, and Sleep

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