NMDA-receptor-dependent plasticity in the bed nucleus of the stria terminalis triggers long-term anxiolysis

Christelle Glangetas, Léma Massi, Giulia R. Fois, Marion Jalabert, Delphine Girard, Marco Diana, Keisuke Yonehara, Botond Roska, Chun Xu, Andreas Lüthi, Stéphanie Caille and François Georges ()
Additional contact information
Christelle Glangetas: Université de Bordeaux, Interdisciplinary Institute for Neuroscience
Léma Massi: Friedrich Miescher Institute for Biomedical Research
Giulia R. Fois: Centre National de la Recherche Scientifique, Neurodegeneratives Diseases Institute
Marion Jalabert: Université de la Méditerranée UMR S901
Delphine Girard: Université de Bordeaux, Interdisciplinary Institute for Neuroscience
Marco Diana: ‘G. Minardi’ Cognitive Neuroscience Laboratory, University of Sassari
Keisuke Yonehara: Friedrich Miescher Institute for Biomedical Research
Botond Roska: Friedrich Miescher Institute for Biomedical Research
Chun Xu: Friedrich Miescher Institute for Biomedical Research
Andreas Lüthi: Friedrich Miescher Institute for Biomedical Research
Stéphanie Caille: Université de Bordeaux, Institut de Neurosciences Cognitives et Intégrative d’Aquitaine, BP31
François Georges: Université de Bordeaux, Interdisciplinary Institute for Neuroscience

Nature Communications, 2017, vol. 8, issue 1, 1-7

Abstract: Abstract Anxiety is controlled by multiple neuronal circuits that share robust and reciprocal connections with the bed nucleus of the stria terminalis (BNST), a key structure controlling negative emotional states. However, it remains unknown how the BNST integrates diverse inputs to modulate anxiety. In this study, we evaluated the contribution of infralimbic cortex (ILCx) and ventral subiculum/CA1 (vSUB/CA1) inputs in regulating BNST activity at the single-cell level. Using trans-synaptic tracing from single-electroporated neurons and in vivo recordings, we show that vSUB/CA1 stimulation promotes opposite forms of in vivo plasticity at the single-cell level in the anteromedial part of the BNST (amBNST). We find that an NMDA-receptor-dependent homosynaptic long-term potentiation is instrumental for anxiolysis. These findings suggest that the vSUB/CA1-driven LTP in the amBNST is involved in eliciting an appropriate response to anxiogenic context and dysfunction of this compensatory mechanism may underlie pathologic anxiety states.

Date: 2017
References: Add references at CitEc
Citations: View citations in EconPapers (2)

Downloads: (external link)
https://www.nature.com/articles/ncomms14456 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14456

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms14456

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().