Hippocampal CB1 Receptors Control Incidental Associations.

Arnau Busquets-Garcia, José F. Oliveira da Cruz, Geoffrey Terral, Antonio C. Pagano Zottola, Edgar Soria-Gómez, Andrea Contini, Hugo Martin, Bastien Redon, Marjorie Varilh, Christina Ioannidou, Filippo Drago, Federico Massa, Xavier Fioramonti, Pierre Trifilieff, Guillaume Ferreira, Giovanni Marsicano
Neuron. 2018-09-01; 99(6): 1247-1259.e7
DOI: 10.1016/j.neuron.2018.08.014

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1. Neuron. 2018 Sep 19;99(6):1247-1259.e7. doi: 10.1016/j.neuron.2018.08.014. Epub
2018 Aug 30.

Hippocampal CB1 Receptors Control Incidental Associations.

Busquets-Garcia A(1), Oliveira da Cruz JF(2), Terral G(1), Zottola ACP(1),
Soria-Gómez E(3), Contini A(4), Martin H(4), Redon B(1), Varilh M(1), Ioannidou
C(1), Drago F(5), Massa F(1), Fioramonti X(4), Trifilieff P(4), Ferreira G(6),
Marsicano G(7).

Author information:
(1)INSERM, U1215 NeuroCentre Magendie, 33000 Bordeaux, France; University of
Bordeaux, 33000 Bordeaux, France.
(2)INSERM, U1215 NeuroCentre Magendie, 33000 Bordeaux, France; University of
Bordeaux, 33000 Bordeaux, France; Department of Biomedical and Biotechnological
Sciences, Section of Pharmacology, University of Catania, I-95123 Catania, Italy.
(3)INSERM, U1215 NeuroCentre Magendie, 33000 Bordeaux, France; University of
Bordeaux, 33000 Bordeaux, France; Department of Neurosciences, University of the
Basque Country UPV/EHU, Achucarro Basque Center for Neuroscience, 48940 Leioa,
Spain; IKERBASQUE, Basque Foundation for Science, 48013 Bilbao, Spain.
(4)University of Bordeaux, 33000 Bordeaux, France; INRA, Nutrition and
Integrative Neurobiology, UMR 1286, Bordeaux, France.
(5)Department of Biomedical and Biotechnological Sciences, Section of
Pharmacology, University of Catania, I-95123 Catania, Italy.
(6)University of Bordeaux, 33000 Bordeaux, France; INRA, Nutrition and
Integrative Neurobiology, UMR 1286, Bordeaux, France. Electronic address:
*protected email*.
(7)INSERM, U1215 NeuroCentre Magendie, 33000 Bordeaux, France; University of
Bordeaux, 33000 Bordeaux, France. Electronic address:
*protected email*.

By priming brain circuits, associations between low-salience stimuli often guide
future behavioral choices through a process known as mediated or inferred
learning. However, the precise neurobiological mechanisms of these incidental
associations are largely unknown. Using sensory preconditioning procedures, we
show that type 1 cannabinoid receptors (CB1R) in hippocampal GABAergic neurons
are necessary and sufficient for mediated but not direct learning. Deletion and
re-expression of CB1R in hippocampal GABAergic neurons abolishes and rescues
mediated learning, respectively. Interestingly, paired presentations of
low-salience sensory cues induce a specific protein synthesis-dependent
enhancement of hippocampal CB1R expression and facilitate long-term synaptic
plasticity at inhibitory synapses. CB1R blockade or chemogenetic manipulations of
hippocampal GABAergic neurons upon preconditioning affect incidental
associations, as revealed by impaired mediated learning. Thus, CB1R-dependent
control of inhibitory hippocampal neurotransmission mediates incidental
associations, allowing future associative inference, a fundamental process for
everyday life, which is altered in major neuropsychiatric diseases. VIDEO
ABSTRACT.

Copyright © 2018 Elsevier Inc. All rights reserved.

DOI: 10.1016/j.neuron.2018.08.014
PMID: 30174119


Auteurs Bordeaux Neurocampus