ArticlePloS one2010
A homolog of FHM2 is involved in modulation of excitatory neurotransmission by serotonin in C. elegans.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
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- Antiaging, Stress Resistance, and Neuroprotective Efficacies ofOxidative medicine and cellular longevity · 2019Article
- Ultraviolet-A triggers photoaging in model nematode Caenorhabditis elegans in a DAF-16 dependent pathway.Age (Dordrecht, Netherlands) · 2016Article
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- A novel cholinergic action of alcohol and the development of tolerance to that effect in Caenorhabditis elegans.Genetics · 2015Article
- VAV-1 acts in a single interneuron to inhibit motor circuit activity in Caenorhabditis elegans.Nature communications · 2014Article
- Phospholipase C activity increases in cerebrospinal fluid from migraineurs in proportion to the number of comorbid conditions: a case-control study.The journal of headache and pain · 2013Article
- Invertebrate models of dystonia.Current neuropharmacology · 2013Article
- Neurite sprouting and synapse deterioration in the aging Caenorhabditis elegans nervous system.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- STR-33, a novel G protein-coupled receptor that regulates locomotion and egg laying in Caenorhabditis elegans.The Journal of biological chemistry · 2011Article
- A genetic survey of fluoxetine action on synaptic transmission in Caenorhabditis elegans.Genetics · 2010Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The C. elegans eat-6 gene encodes a Na(+), K(+)-ATPase alpha subunit and is a homolog of the familial hemiplegic migraine candidate gene FHM2. Migraine is the most common neurological disorder linked to serotonergic dysfunction. We sought to study the pathophysiological mechanisms of migraine and their relation to serotonin (5-HT) signaling using C. elegans as a genetic model. In C. elegans, exogenous 5-HT inhibits paralysis induced by the acetylcholinesterase inhibitor aldicarb. We found that the eat-6(ad467) mutation or RNAi of eat-6 increases aldicarb sensitivity and causes complete resistance to 5-HT treatment, indicating that EAT-6 is a component of the pathway that couples 5-HT signaling and ACh neurotransmission. While a postsynaptic role of EAT-6 at the bodywall NMJs has been well established, we found that EAT-6 may in addition regulate presynaptic ACh neurotransmission. We show that eat-6 is expressed in ventral cord ACh motor neurons, and that cell-specific RNAi of eat-6 in the ACh neurons leads to hypersensitivity to aldicarb. Electron microscopy showed an increased number of synaptic vesicles in the ACh neurons in the eat-6(ad467) mutant. Genetic analyses suggest that EAT-6 interacts with EGL-30 Galphaq, EGL-8 phospholipase C and SLO-1 BK channel signaling to modulate ACh neurotransmission and that either reduced or excessive EAT-6 function may lead to increased ACh neurotransmission. Study of the interaction between eat-6 and 5-HT receptors revealed both stimulatory and inhibitory 5-HT inputs to the NMJs. We show that the inhibitory and stimulatory 5-HT signals arise from distinct 5-HT neurons. The role of eat-6 in modulation of excitatory neurotransmission by 5-HT may provide a genetic explanation for the therapeutic effects of the drugs targeting 5-HT receptors in the treatment of migraine patients.
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