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GPA-14, a Gα(i) subunit mediates dopaminergic behavioral plasticity in C. elegans
BACKGROUND: Precise levels of specific neurotransmitters are required for appropriate neuronal functioning. The neurotransmitter dopamine is implicated in modulating behaviors, such as cognition, reward and memory. In the nematode Caenorhabditis elegans, the release of dopamine during behavioral pla...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3679979/ https://www.ncbi.nlm.nih.gov/pubmed/23607404 http://dx.doi.org/10.1186/1744-9081-9-16 |
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author | Mersha, Mahlet Formisano, Rosaria McDonald, Rochelle Pandey, Pratima Tavernarakis, Nektarios Harbinder, Singh |
author_facet | Mersha, Mahlet Formisano, Rosaria McDonald, Rochelle Pandey, Pratima Tavernarakis, Nektarios Harbinder, Singh |
author_sort | Mersha, Mahlet |
collection | PubMed |
description | BACKGROUND: Precise levels of specific neurotransmitters are required for appropriate neuronal functioning. The neurotransmitter dopamine is implicated in modulating behaviors, such as cognition, reward and memory. In the nematode Caenorhabditis elegans, the release of dopamine during behavioral plasticity is in part modulated through an acid-sensing ion channel expressed in its eight dopaminergic neurons. A D2-like C. elegans dopamine receptor DOP-2 co-expresses along with a Gα(i) subunit (GPA-14) in the anterior deirid (ADE) pair of dopaminergic neurons. FINDINGS: In follow-up experiments to our recently reported in vitro physical interaction between DOP-2 and GPA-14, we have behaviorally characterized worms carrying deletion mutations in gpa-14 and/or dop-2. We found both mutants to display behavioral abnormalities in habituation as well as associative learning, and exogenous supply of dopamine was able to revert the observed behavioral deficits. The behavioral phenotypes of dop-2 and gpa-14 loss-of-function mutants were found to be remarkably similar, and we did not observe any cumulative defects in their double mutants. CONCLUSION: Our results provide genetic and phenotypic support to our earlier in vitro results where we had shown that the DOP-2 dopamine receptor and the GPA-14 Gα(i) subunit physically interact with each other. Results from behavioral experiments presented here together with our previous in-vitro work suggests that the DOP-2 functions as a dopamine auto-receptor to modulate two types of learning, anterior touch habituation and chemosensory associative conditioning, through a G-protein complex that comprises GPA-14 as its Gα subunit. |
format | Online Article Text |
id | pubmed-3679979 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-36799792013-06-13 GPA-14, a Gα(i) subunit mediates dopaminergic behavioral plasticity in C. elegans Mersha, Mahlet Formisano, Rosaria McDonald, Rochelle Pandey, Pratima Tavernarakis, Nektarios Harbinder, Singh Behav Brain Funct Short Paper BACKGROUND: Precise levels of specific neurotransmitters are required for appropriate neuronal functioning. The neurotransmitter dopamine is implicated in modulating behaviors, such as cognition, reward and memory. In the nematode Caenorhabditis elegans, the release of dopamine during behavioral plasticity is in part modulated through an acid-sensing ion channel expressed in its eight dopaminergic neurons. A D2-like C. elegans dopamine receptor DOP-2 co-expresses along with a Gα(i) subunit (GPA-14) in the anterior deirid (ADE) pair of dopaminergic neurons. FINDINGS: In follow-up experiments to our recently reported in vitro physical interaction between DOP-2 and GPA-14, we have behaviorally characterized worms carrying deletion mutations in gpa-14 and/or dop-2. We found both mutants to display behavioral abnormalities in habituation as well as associative learning, and exogenous supply of dopamine was able to revert the observed behavioral deficits. The behavioral phenotypes of dop-2 and gpa-14 loss-of-function mutants were found to be remarkably similar, and we did not observe any cumulative defects in their double mutants. CONCLUSION: Our results provide genetic and phenotypic support to our earlier in vitro results where we had shown that the DOP-2 dopamine receptor and the GPA-14 Gα(i) subunit physically interact with each other. Results from behavioral experiments presented here together with our previous in-vitro work suggests that the DOP-2 functions as a dopamine auto-receptor to modulate two types of learning, anterior touch habituation and chemosensory associative conditioning, through a G-protein complex that comprises GPA-14 as its Gα subunit. BioMed Central 2013-04-22 /pmc/articles/PMC3679979/ /pubmed/23607404 http://dx.doi.org/10.1186/1744-9081-9-16 Text en Copyright © 2013 Mersha et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Short Paper Mersha, Mahlet Formisano, Rosaria McDonald, Rochelle Pandey, Pratima Tavernarakis, Nektarios Harbinder, Singh GPA-14, a Gα(i) subunit mediates dopaminergic behavioral plasticity in C. elegans |
title | GPA-14, a Gα(i) subunit mediates dopaminergic behavioral plasticity in C. elegans |
title_full | GPA-14, a Gα(i) subunit mediates dopaminergic behavioral plasticity in C. elegans |
title_fullStr | GPA-14, a Gα(i) subunit mediates dopaminergic behavioral plasticity in C. elegans |
title_full_unstemmed | GPA-14, a Gα(i) subunit mediates dopaminergic behavioral plasticity in C. elegans |
title_short | GPA-14, a Gα(i) subunit mediates dopaminergic behavioral plasticity in C. elegans |
title_sort | gpa-14, a gα(i) subunit mediates dopaminergic behavioral plasticity in c. elegans |
topic | Short Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3679979/ https://www.ncbi.nlm.nih.gov/pubmed/23607404 http://dx.doi.org/10.1186/1744-9081-9-16 |
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