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GluA1 AMPAR subunit deletion reduces the hedonic response to sucrose but leaves satiety and conditioned responses intact
The GluA1 subunit of the AMPA receptor has been implicated in schizophrenia. While GluA1 is important for cognition, it is not clear what the role of GluA1 is in hedonic responses that are relevant to the negative symptoms of disorders such as schizophrenia. Here, we tested mice that lack GluA1 (Gri...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547105/ https://www.ncbi.nlm.nih.gov/pubmed/28785046 http://dx.doi.org/10.1038/s41598-017-07542-9 |
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author | Austen, Joseph M. Sprengel, Rolf Sanderson, David J. |
author_facet | Austen, Joseph M. Sprengel, Rolf Sanderson, David J. |
author_sort | Austen, Joseph M. |
collection | PubMed |
description | The GluA1 subunit of the AMPA receptor has been implicated in schizophrenia. While GluA1 is important for cognition, it is not clear what the role of GluA1 is in hedonic responses that are relevant to the negative symptoms of disorders such as schizophrenia. Here, we tested mice that lack GluA1 (Gria1 (−/−) mice) on consumption of sucrose solutions using a licking microstructure analysis. GluA1 deletion drastically reduced palatability (as measured by the mean lick cluster size) across a range of sucrose concentrations. Although initial lick rates were reduced, measures of consumption across long periods of access to sucrose solutions were not affected by GluA1 deletion and Gria1 (−/−) mice showed normal satiety responses to high sucrose concentrations. GluA1 deletion also failed to impair flavour conditioning, in which increased intake of a flavour occurred as a consequence of prior pairing with a high sucrose concentration. These results demonstrate that GluA1 plays a role in responding on the basis of palatability rather than other properties, such as the automatic and learnt post-ingestive, nutritional consequences of sucrose. Therefore, Gria1 (−/−) mice provide a potential model of anhedonia, adding converging evidence to the role of glutamatergic dysfunction in various symptoms of schizophrenia and related disorders. |
format | Online Article Text |
id | pubmed-5547105 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-55471052017-08-09 GluA1 AMPAR subunit deletion reduces the hedonic response to sucrose but leaves satiety and conditioned responses intact Austen, Joseph M. Sprengel, Rolf Sanderson, David J. Sci Rep Article The GluA1 subunit of the AMPA receptor has been implicated in schizophrenia. While GluA1 is important for cognition, it is not clear what the role of GluA1 is in hedonic responses that are relevant to the negative symptoms of disorders such as schizophrenia. Here, we tested mice that lack GluA1 (Gria1 (−/−) mice) on consumption of sucrose solutions using a licking microstructure analysis. GluA1 deletion drastically reduced palatability (as measured by the mean lick cluster size) across a range of sucrose concentrations. Although initial lick rates were reduced, measures of consumption across long periods of access to sucrose solutions were not affected by GluA1 deletion and Gria1 (−/−) mice showed normal satiety responses to high sucrose concentrations. GluA1 deletion also failed to impair flavour conditioning, in which increased intake of a flavour occurred as a consequence of prior pairing with a high sucrose concentration. These results demonstrate that GluA1 plays a role in responding on the basis of palatability rather than other properties, such as the automatic and learnt post-ingestive, nutritional consequences of sucrose. Therefore, Gria1 (−/−) mice provide a potential model of anhedonia, adding converging evidence to the role of glutamatergic dysfunction in various symptoms of schizophrenia and related disorders. Nature Publishing Group UK 2017-08-07 /pmc/articles/PMC5547105/ /pubmed/28785046 http://dx.doi.org/10.1038/s41598-017-07542-9 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Austen, Joseph M. Sprengel, Rolf Sanderson, David J. GluA1 AMPAR subunit deletion reduces the hedonic response to sucrose but leaves satiety and conditioned responses intact |
title | GluA1 AMPAR subunit deletion reduces the hedonic response to sucrose but leaves satiety and conditioned responses intact |
title_full | GluA1 AMPAR subunit deletion reduces the hedonic response to sucrose but leaves satiety and conditioned responses intact |
title_fullStr | GluA1 AMPAR subunit deletion reduces the hedonic response to sucrose but leaves satiety and conditioned responses intact |
title_full_unstemmed | GluA1 AMPAR subunit deletion reduces the hedonic response to sucrose but leaves satiety and conditioned responses intact |
title_short | GluA1 AMPAR subunit deletion reduces the hedonic response to sucrose but leaves satiety and conditioned responses intact |
title_sort | glua1 ampar subunit deletion reduces the hedonic response to sucrose but leaves satiety and conditioned responses intact |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5547105/ https://www.ncbi.nlm.nih.gov/pubmed/28785046 http://dx.doi.org/10.1038/s41598-017-07542-9 |
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