Circuit specific functions of cannabinoid CB1 receptor in the balance of investigatory drive and exploration.

Well balanced novelty seeking and exploration are fundamental behaviours for survival and are found to be dysfunctional in several psychiatric disorders. Recent studies suggest that the endocannabinoid (eCB) system is an important control system for investigatory drive. Pharmacological treatment of...

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Autores principales: Martin Häring, Nadine Kaiser, Krisztina Monory, Beat Lutz
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Publicado: Public Library of Science (PLoS) 2011
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Acceso en línea:https://doaj.org/article/b2426a914fdf4062b15e035e41c3103e
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spelling oai:doaj.org-article:b2426a914fdf4062b15e035e41c3103e2021-11-18T07:35:18ZCircuit specific functions of cannabinoid CB1 receptor in the balance of investigatory drive and exploration.1932-620310.1371/journal.pone.0026617https://doaj.org/article/b2426a914fdf4062b15e035e41c3103e2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22069458/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Well balanced novelty seeking and exploration are fundamental behaviours for survival and are found to be dysfunctional in several psychiatric disorders. Recent studies suggest that the endocannabinoid (eCB) system is an important control system for investigatory drive. Pharmacological treatment of rodents with cannabinergic drugs results in altered social and object investigation. Interestingly, contradictory results have been obtained, depending on the treatment, drug concentration and experimental conditions. The cannabinoid type 1 (CB1) receptor, a central component of the eCB system, is predominantly found at the synapses of two opposing neuronal populations, i.e. on inhibitory GABAergic and excitatory glutamatergic neurons. In the present study, using different transgenic mouse lines, we aimed at investigating the impact of CB1 receptor inactivation in glutamatergic or GABAergic neurons on investigatory behaviour. We evaluated animate (interaction partner) and inanimate (object) exploratory behaviour in three different paradigms. We show that exploration was increased when CB1 receptor was deleted from cortical and striatal GABAergic neurons. No effect was observed when CB1 receptor was deleted specifically from dopamine receptor D1-expressing striatal GABAergic medium spiny neurons. In contrast, deletion of CB1 receptor from cortical glutamatergic neurons resulted in a decreased exploration. Thus, our results indicate that exploratory behaviour is accurately balanced in both, the social and non-social context, by the eCB system via CB1 receptor activation on cortical glutamatergic and GABAergic neurons. In addition, the results could explain the contradictory findings of previous pharmacological studies and could further suggest a possibility to readjust an imbalance in exploratory behaviour observed in psychiatric disorders.Martin HäringNadine KaiserKrisztina MonoryBeat LutzPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 11, p e26617 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Martin Häring
Nadine Kaiser
Krisztina Monory
Beat Lutz
Circuit specific functions of cannabinoid CB1 receptor in the balance of investigatory drive and exploration.
description Well balanced novelty seeking and exploration are fundamental behaviours for survival and are found to be dysfunctional in several psychiatric disorders. Recent studies suggest that the endocannabinoid (eCB) system is an important control system for investigatory drive. Pharmacological treatment of rodents with cannabinergic drugs results in altered social and object investigation. Interestingly, contradictory results have been obtained, depending on the treatment, drug concentration and experimental conditions. The cannabinoid type 1 (CB1) receptor, a central component of the eCB system, is predominantly found at the synapses of two opposing neuronal populations, i.e. on inhibitory GABAergic and excitatory glutamatergic neurons. In the present study, using different transgenic mouse lines, we aimed at investigating the impact of CB1 receptor inactivation in glutamatergic or GABAergic neurons on investigatory behaviour. We evaluated animate (interaction partner) and inanimate (object) exploratory behaviour in three different paradigms. We show that exploration was increased when CB1 receptor was deleted from cortical and striatal GABAergic neurons. No effect was observed when CB1 receptor was deleted specifically from dopamine receptor D1-expressing striatal GABAergic medium spiny neurons. In contrast, deletion of CB1 receptor from cortical glutamatergic neurons resulted in a decreased exploration. Thus, our results indicate that exploratory behaviour is accurately balanced in both, the social and non-social context, by the eCB system via CB1 receptor activation on cortical glutamatergic and GABAergic neurons. In addition, the results could explain the contradictory findings of previous pharmacological studies and could further suggest a possibility to readjust an imbalance in exploratory behaviour observed in psychiatric disorders.
format article
author Martin Häring
Nadine Kaiser
Krisztina Monory
Beat Lutz
author_facet Martin Häring
Nadine Kaiser
Krisztina Monory
Beat Lutz
author_sort Martin Häring
title Circuit specific functions of cannabinoid CB1 receptor in the balance of investigatory drive and exploration.
title_short Circuit specific functions of cannabinoid CB1 receptor in the balance of investigatory drive and exploration.
title_full Circuit specific functions of cannabinoid CB1 receptor in the balance of investigatory drive and exploration.
title_fullStr Circuit specific functions of cannabinoid CB1 receptor in the balance of investigatory drive and exploration.
title_full_unstemmed Circuit specific functions of cannabinoid CB1 receptor in the balance of investigatory drive and exploration.
title_sort circuit specific functions of cannabinoid cb1 receptor in the balance of investigatory drive and exploration.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/b2426a914fdf4062b15e035e41c3103e
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