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Rewarding Social Interaction in Rats Increases CaMKII in the Nucleus Accumbens
Calcium/calmodulin-dependent protein kinase II (CaMKII) is known to be involved in the sensitized locomotor responses and drug-seeking behavior to psychostimulants. However, little is known about the contribution of CaMKII signaling in the nucleus accumbens (NAc) in natural rewards such as social in...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8698734/ https://www.ncbi.nlm.nih.gov/pubmed/34944702 http://dx.doi.org/10.3390/biomedicines9121886 |
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author | Amaral, Inês M. Scheffauer, Laura Langeder, Angelika B. Hofer, Alex El Rawas, Rana |
author_facet | Amaral, Inês M. Scheffauer, Laura Langeder, Angelika B. Hofer, Alex El Rawas, Rana |
author_sort | Amaral, Inês M. |
collection | PubMed |
description | Calcium/calmodulin-dependent protein kinase II (CaMKII) is known to be involved in the sensitized locomotor responses and drug-seeking behavior to psychostimulants. However, little is known about the contribution of CaMKII signaling in the nucleus accumbens (NAc) in natural rewards such as social interaction. The present experiments explored the implication of CaMKII signaling in drug versus natural reward. In the NAc of rats expressing cocaine or social interaction conditioned place preference (CPP), αCaMKII activation was induced in those expressing social interaction but not cocaine CPP. In order to investigate the role of NAc CaMKII in the expression of reward-related learning of drug versus non-drug stimuli, we inhibited CaMKII through an infusion of KN-93, a CaMKII inhibitor, directly into the NAc shell or core, before the CPP test in a concurrent paradigm in which social interaction was made available in the compartment alternative to the one associated with cocaine during conditioning. Whereas vehicle infusions led to equal preference to both stimuli, inhibition of CaMKII by a KN-93 infusion before the CPP test in the shell but not the core of the NAc shifted the rats’ preference toward the cocaine-associated compartment. Altogether, these results suggest that social interaction reward engages CaMKII in the NAc. |
format | Online Article Text |
id | pubmed-8698734 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-86987342021-12-24 Rewarding Social Interaction in Rats Increases CaMKII in the Nucleus Accumbens Amaral, Inês M. Scheffauer, Laura Langeder, Angelika B. Hofer, Alex El Rawas, Rana Biomedicines Article Calcium/calmodulin-dependent protein kinase II (CaMKII) is known to be involved in the sensitized locomotor responses and drug-seeking behavior to psychostimulants. However, little is known about the contribution of CaMKII signaling in the nucleus accumbens (NAc) in natural rewards such as social interaction. The present experiments explored the implication of CaMKII signaling in drug versus natural reward. In the NAc of rats expressing cocaine or social interaction conditioned place preference (CPP), αCaMKII activation was induced in those expressing social interaction but not cocaine CPP. In order to investigate the role of NAc CaMKII in the expression of reward-related learning of drug versus non-drug stimuli, we inhibited CaMKII through an infusion of KN-93, a CaMKII inhibitor, directly into the NAc shell or core, before the CPP test in a concurrent paradigm in which social interaction was made available in the compartment alternative to the one associated with cocaine during conditioning. Whereas vehicle infusions led to equal preference to both stimuli, inhibition of CaMKII by a KN-93 infusion before the CPP test in the shell but not the core of the NAc shifted the rats’ preference toward the cocaine-associated compartment. Altogether, these results suggest that social interaction reward engages CaMKII in the NAc. MDPI 2021-12-12 /pmc/articles/PMC8698734/ /pubmed/34944702 http://dx.doi.org/10.3390/biomedicines9121886 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Amaral, Inês M. Scheffauer, Laura Langeder, Angelika B. Hofer, Alex El Rawas, Rana Rewarding Social Interaction in Rats Increases CaMKII in the Nucleus Accumbens |
title | Rewarding Social Interaction in Rats Increases CaMKII in the Nucleus Accumbens |
title_full | Rewarding Social Interaction in Rats Increases CaMKII in the Nucleus Accumbens |
title_fullStr | Rewarding Social Interaction in Rats Increases CaMKII in the Nucleus Accumbens |
title_full_unstemmed | Rewarding Social Interaction in Rats Increases CaMKII in the Nucleus Accumbens |
title_short | Rewarding Social Interaction in Rats Increases CaMKII in the Nucleus Accumbens |
title_sort | rewarding social interaction in rats increases camkii in the nucleus accumbens |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8698734/ https://www.ncbi.nlm.nih.gov/pubmed/34944702 http://dx.doi.org/10.3390/biomedicines9121886 |
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