Like many behaviors, Caenorhabditis elegans egg laying alternates between inactive and active states. To understand how the underlying neural circuit turns the behavior on and off, we optically recorded circuit activity in behaving animals while manipulating circuit function using mutations, optogenetics, and drugs. In the active state, the circuit shows rhythmic activity phased with the body bends of locomotion. The serotonergic HSN command neurons initiate the active state, but accumulation of unlaid eggs also promotes the active state independent of the HSNs. The cholinergic VC motor neurons slow locomotion during egg-laying muscle contraction and egg release. The uv1 neuroendocrine cells mechanically sense passage of eggs through the vulva and release tyramine to inhibit egg laying, in part via the LGC-55 tyramine-gated Cl- channel on the HSNs. Our results identify discrete signals that entrain or detach the circuit from the locomotion central pattern generator to produce active and inactive states.DOI:
http://dx.doi.org/10.7554/eLife.21126.001
21Like many behaviors, Caenorhabditis elegans egg laying alternates between inactive and 22 active states. To understand how the underlying neural circuit turns the behavior on and off, we 23 optically recorded circuit activity in behaving animals while manipulating circuit function using 24 mutations, optogenetics, and drugs. In the active state, the circuit shows rhythmic activity 25 phased with the body bends of locomotion. The serotonergic HSN command neurons initiate 26 the active state, but accumulation of unlaid eggs also promotes the active state independent of 27 the HSNs. The cholinergic VC motor neurons slow locomotion during egg-laying muscle 28 contraction and egg release. The uv1 neuroendocrine cells mechanically sense passage of 29 eggs through the vulva and release tyramine to inhibit egg laying, in part via the LGC-55 30 tyramine-gated Clchannel on the HSNs. Our results identify discrete signals that entrain or 31 detach the circuit from the locomotion central pattern generator to produce active and inactive 32
This work was funded by grants from the NIH (R01-NS086932) and NSF (IOS-1844657) to KMC. RJK 3 rd was supported by a University of Miami Maytag Fellowship. We thank David M. Miller III for sharing plasmids. Some of the strains used in this study were provided by the C.
Successful execution of behavior requires the coordinated activity and communication between multiple cell types. Studies using the relatively simple neural circuits of invertebrates have helped to uncover how conserved molecular and cellular signaling events shape animal behavior. To understand the mechanisms underlying neural circuit activity and behavior, we have been studying a simple circuit that drives egg-laying behavior in the nematode worm C. elegans. Here we show that the female-specific, Ventral C (VC) motoneurons are required for vulval muscle contractility and egg laying in response to serotonin. Ca2+ imaging experiments show the VCs are active during times of vulval muscle contraction and vulval opening, and optogenetic stimulation of the VCs promotes vulval muscle Ca2+ activity. However, while silencing of the VCs does not grossly affect steady-state egg-laying behavior, VC silencing does block egg laying in response to serotonin and increases the failure rate of egg-laying attempts. Signaling from the VCs facilitates full vulval muscle contraction and opening of the vulva for efficient egg laying. We also find the VCs are mechanically activated in response to vulval opening. Optogenetic stimulation of the vulval muscles is sufficient to drive VC Ca2+ activity and requires muscle contractility, showing the presynaptic VCs and the postsynaptic vulval muscles can mutually excite each other. Together, our results demonstrate that the VC neurons facilitate efficient execution of egg-laying behavior by coordinating postsynaptic muscle contractility in response to serotonin and mechanosensory feedback.
C. elegans worms encountering Cu2O particles can either avoid and survive or they can ingest them and experience toxic effects. Phosphate induces particle oxidation and Cu ion precipitation, improving survival even after ingestion.
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