ArticlePLoS genetics2019
Serotonin and neuropeptides are both released by the HSN command neuron to initiate Caenorhabditis elegans egg laying.
Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 72 citations in OpenAlex.
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- Neuropeptide and serotonin co-transmission sets the activity pattern in the C. elegans egg-laying circuit.Current biology : CB · 2024Article
- Neuropeptide inactivation regulates egg-laying behavior to influence reproductive health in Caenorhabditis elegans.Current biology : CB · 2024Article
- Novel C. elegans models of Lewy body disease reveal pathological protein interactions and widespread miRNA dysregulation.Cellular and molecular life sciences : CMLS · 2024Article
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- A single neuron in C. elegans orchestrates multiple motor outputs through parallel modes of transmission.Current biology : CB · 2023Article
- End-binding protein 1 promotes specific motor-cargo association in the cell body prior to axonal delivery of dense core vesicles.Current biology : CB · 2023Article
- Multiple Subthreshold GPCR Signals Combined by the G-Proteins GαThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Neurons typically release both a small-molecule neurotransmitter and one or more neuropeptides, but how these two types of signal from the same neuron might act together remains largely obscure. For example, serotonergic neurons in mammalian brain express the neuropeptide Substance P, but it is unclear how this co-released neuropeptide might modulate serotonin signaling. We studied this issue in C. elegans, in which all serotonergic neurons express the neuropeptide NLP-3. The serotonergic Hermaphrodite Specific Neurons (HSNs) are command motor neurons within the egg-laying circuit which have been shown to release serotonin to initiate egg-laying behavior. We found that egg-laying defects in animals lacking serotonin were far milder than in animals lacking HSNs, suggesting that HSNs must release other signal(s) in addition to serotonin to stimulate egg laying. While null mutants for nlp-3 had only mild egg-laying defects, animals lacking both serotonin and NLP-3 had severe defects, similar to those of animals lacking HSNs. Optogenetic activation of HSNs induced egg laying in wild-type animals, and in mutant animals lacking either serotonin or NLP-3, but failed to induce egg laying in animals lacking both. We recorded calcium activity in the egg-laying muscles of animals lacking either serotonin, NLP-3, or both. The single mutants, and to a greater extent the double mutant, showed muscle activity that was uncoordinated and unable to expel eggs. Specifically, the vm2 muscles cells, which are direct postsynaptic targets of the HSN, failed to contract simultaneously with other egg-laying muscle cells. Our results show that the HSN neurons use serotonin and the neuropeptide NLP-3 as partially redundant co-transmitters that together stimulate and coordinate activity of the target cells onto which they are released.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.