Activity of theC. elegansegg-laying behavior circuit is controlled by competing activation and feedback inhibition

Abstract

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

Sexual Dimorphism and Sex Differences in Caenorhabditis elegans Neuronal Development and Behavior

“…The VC neurons also activate inhibitory G ao -coupled GAR-2 receptors on the HSN, suggesting that VC neurons can also fine-tune HSN activity within the active phase (Bany et al 2003;Zhang et al 2010). The coupling of locomotion to egg laying not only facilitates the dispersal of progeny, but also allows the body wall muscle contractions to aid the uterine muscles in egg expulsion (Collins and Koelle 2013;Collins et al 2016).…”

Distinct unfolded protein responses mitigate or mediate effects of nonlethal deprivation of C. elegans sleep in different tissues

“…The absence of hermaphrodite-specific neurons (HSNs) suppresses egg laying and doubles the frequency of calcium transients in vulval muscles (vms) [ 83 , 102 ]. As germ cell apoptosis does not preclude an independent impact of deprivation on the egg-laying circuit, we asked whether sleep deprivation can cause abnormally high calcium activity in the vms.…”

“…As germ cell apoptosis does not preclude an independent impact of deprivation on the egg-laying circuit, we asked whether sleep deprivation can cause abnormally high calcium activity in the vms. To address this, we assayed calcium dynamics indicative of vm twitching using a ratiometric reporter: co-expression of the calcium indicator GCaMP5 and the red fluorescent protein mCherry in the vms [ 83 , 103 ] (Fig. 8a , b ).…”

“…Physiological activity in the egg-laying circuit is coupled with body posture and locomotion during brief periods around egg-laying events [ 83 , 103 , 104 ]. Therefore, we could not rule out the possibility that differences in locomotion over long timescales may also correlate with activity in the egg-laying circuit.…”

“…In addition, the egg-laying circuit exhibited a post-deprivation defect similar to the outcome of genetically ablating an egg-laying command neuron [ 83 ]. Opposite to the case of the feeding circuit, the UPR ER (but not the UPR mt ) mitigated the impact of deprivation in the egg-laying circuit.…”