Genetic and pharmacological analysis of neurotransmitters controlling egg laying in C. elegans

Weinshenker, David; Garriga, Gian; Thomas, JH

doi:10.1523/jneurosci.15-10-06975.1995

Cited by 200 publications

(216 citation statements)

References 27 publications

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“…The egl-2(gf) allele induces egg retention in hermaphrodites as well as defecation and chemotaxis defects (Reiner et al 1995;Weinshenker et al 1995; Mean gray level of DsRed-E5 fluorescent protein expression in the male tail. DsRed-E5 initially expresses in the green channel and then shifts its emission spectra to the red channel.…”

Section: Resultsmentioning

confidence: 99%

Cell Excitability Necessary for Male Mating Behavior inCaenorhabditis elegansIs Coordinated by Interactions Between Big Current and Ether-A-Go-Go Family K+ Channels

LeBoeuf

García

2012

Genetics

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Variations in K + channel composition allow for differences in cell excitability and, at an organismal level, provide flexibility to behavioral regulation. When the function of a K + channel is disrupted, the remaining K + channels might incompletely compensate, manifesting as abnormal organismal behavior. In this study, we explored how different K + channels interact to regulate the neuromuscular circuitry used by Caenorhabditis elegans males to protract their copulatory spicules from their tail and insert them into the hermaphrodite's vulva during mating. We determined that the big current K + channel (BK)/SLO-1 genetically interacts with ether-a-gogo (EAG)/EGL-2 and EAG-related gene/UNC-103 K + channels to control spicule protraction. Through rescue experiments, we show that specific slo-1 isoforms affect spicule protraction. Gene expression studies show that slo-1 and egl-2 expression can be upregulated in a calcium/calmodulin-dependent protein kinase II-dependent manner to compensate for the loss of unc-103 and conversely, unc-103 can partially compensate for the loss of SLO-1 function. In conclusion, an interaction between BK and EAG family K + channels produces the muscle excitability levels that regulate the timing of spicule protraction and the success of male mating behavior.

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Section: Resultsmentioning

confidence: 99%

Cell Excitability Necessary for Male Mating Behavior inCaenorhabditis elegansIs Coordinated by Interactions Between Big Current and Ether-A-Go-Go Family K+ Channels

LeBoeuf

García

2012

Genetics

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“…None of these drugs appreciably inhibited DAF-16::GFP nuclear accumulation. Weinshenker et al (39) demonstrated that fluoxetine is taken up by C. elegans, and all of these control drugs can cross the blood-brain barrier in mammals.…”

Section: Resultsmentioning

confidence: 99%

Antipsychotic Drugs Activate the C. elegans Akt Pathway via the DAF-2 Insulin/IGF-1 Receptor

Weeks

Dwyer

Aamodt

2010

ACS Chem. Neurosci.

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The molecular modes of action of antipsychotic drugs are poorly understood beyond their effects at the dopamine D2 receptor. Previous studies have placed Akt signaling downstream of D2 dopamine receptors, and recent data have suggested an association between psychotic illnesses and defective Akt signaling. To characterize the effect of antipsychotic drugs on the Akt pathway, we used the model organism C. elegans, a simple system where the Akt/forkhead box O transcription factor (FOXO) pathway has been well characterized. All major classes of antipsychotic drugs increased signaling through the insulin/Akt/FOXO pathway, whereas four other drugs that are known to affect the central nervous system did not. The antipsychotic drugs inhibited dauer formation, dauer recovery, and shortened lifespan, three biological processes affected by Akt signaling. Genetic analysis showed that AKT-1 and the insulin and insulin-like growth factor receptor, DAF-2, were required for the antipsychotic drugs to increase signaling. Serotonin synthesis was partially involved, whereas the mitogen activated protein kinase (MAPK), SEK-1 is a MAP kinase kinase (MAPKK), and calcineurin were not involved. This is the first example of a common but specific molecular effect produced by all presently known antipsychotic drugs in any biological system. Because untreated schizophrenics have been reported to have low levels of Akt signaling, increased Akt signaling might contribute to the therapeutic actions of antipsychotic drugs.

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“…Dopamine plays a significant role in C. elegans behaviors, including locomotion, egg laying, and the basal slowing response to food (Schafer and Kenyon, 1995;Weinshenker et al, 1995;Sawin et al, 2000). The C. elegans hermaphrodite has four bilaterally symmetrical pairs of dopaminergic neurons (ADE neurons, PDE neurons, and two pairs of CEP neurons) that appear to play a role in mechanosensation (Sulston et al, 1975;Sawin et al, 2000).…”

Section: Dopaminergic Signaling Is Required For Arsmentioning

confidence: 99%

“…In response to attractive stimuli, such as food, C. elegans modulates its turning frequency and navigates up a gradient of chemical cues (Croll, 1975;Pierce-Shimomura et al, 1999). Dopaminergic signaling mediates the locomotory response to food (Sawin et al, 2000) and also plays a role in feeding and egg laying (Schafer and Kenyon, 1995;Weinshenker et al, 1995). Four pairs of bilaterally symmetrical dopaminergic sensory neurons have been identified in the C. elegans hermaphrodite (Sulston et al, 1975).…”

Section: Introductionmentioning

confidence: 99%

Dopamine and Glutamate Control Area-Restricted Search Behavior inCaenorhabditis elegans

Hills

Brockie

Maricq³

2004

J. Neurosci.

320

354

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Area-restricted search (ARS) is a foraging strategy used by many animals to locate resources. The behavior is characterized by a timedependent reduction in turning frequency after the last resource encounter. This maximizes the time spent in areas in which resources are abundant and extends the search to a larger area when resources become scarce. We demonstrate that dopaminergic and glutamatergic signaling contribute to the neural circuit controlling ARS in the nematode Caenorhabditis elegans. Ablation of dopaminergic neurons eliminated ARS behavior, as did application of the dopamine receptor antagonist raclopride. Furthermore, ARS was affected by mutations in the glutamate receptor subunits GLR-1 and GLR-2 and the EAT-4 glutamate vesicular transporter. Interestingly, preincubation on dopamine restored the behavior in worms with defective dopaminergic signaling, but not in glr-1, glr-2, or eat-4 mutants. This suggests that dopaminergic and glutamatergic signaling function in the same pathway to regulate turn frequency. Both GLR-1 and GLR-2 are expressed in the locomotory control circuit that modulates the direction of locomotion in response to sensory stimuli and the duration of forward movement during foraging. We propose a mechanism for ARS in C. elegans in which dopamine, released in response to food, modulates glutamatergic signaling in the locomotory control circuit, thus resulting in an increased turn frequency.

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Genetic and pharmacological analysis of neurotransmitters controlling egg laying in C. elegans

Cited by 200 publications

References 27 publications

Cell Excitability Necessary for Male Mating Behavior inCaenorhabditis elegansIs Coordinated by Interactions Between Big Current and Ether-A-Go-Go Family K+ Channels

Cell Excitability Necessary for Male Mating Behavior inCaenorhabditis elegansIs Coordinated by Interactions Between Big Current and Ether-A-Go-Go Family K+ Channels

Antipsychotic Drugs Activate the C. elegans Akt Pathway via the DAF-2 Insulin/IGF-1 Receptor

Dopamine and Glutamate Control Area-Restricted Search Behavior inCaenorhabditis elegans

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