NMDA-receptor-dependent plasticity in the bed nucleus of the stria terminalis triggers long-term anxiolysis.
Nat Comms. 2017-02-20; 8: 14456
DOI: 10.1038/ncomms14456
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1. Nat Commun. 2017 Feb 20;8:14456. doi: 10.1038/ncomms14456.
NMDA-receptor-dependent plasticity in the bed nucleus of the stria terminalis
triggers long-term anxiolysis.
Glangetas C(1)(2), Massi L(3), Fois GR(4), Jalabert M(5)(6), Girard D(1)(2)(4),
Diana M(7), Yonehara K(3), Roska B(3), Xu C(3), Lüthi A(3), Caille S(8)(9),
Georges F(1)(2)(4).
Author information:
(1)Université de Bordeaux, Interdisciplinary Institute for Neuroscience, UMR
5297, F-33076 Bordeaux, France.
(2)Centre National de la Recherche Scientifique, Interdisciplinary Institute for
Neuroscience, UMR 5297, F-33076 Bordeaux, France.
(3)Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, 4058
Basel, Switzerland.
(4)Centre National de la Recherche Scientifique, Neurodegeneratives Diseases
Institute, UMR 5293, F-33076 Bordeaux, France.
(5)Université de la Méditerranée UMR S901, F-13009 Aix-Marseille 2, France.
(6)INMED, F-13009 Marseille, France.
(7)’G. Minardi’ Cognitive Neuroscience Laboratory, Department of Chemistry and
Pharmacy, University of Sassari, 07100 Sassari, Italy.
(8)Université de Bordeaux, Institut de Neurosciences Cognitives et Intégrative
d’Aquitaine, BP31, F-33076 Bordeaux, France.
(9)Centre National de la Recherche Scientifique, UMR 5287-Institut de
Neurosciences Cognitives et Intégrative d’Aquitaine, F-33076 Bordeaux, France.
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.
DOI: 10.1038/ncomms14456
PMCID: PMC5321732
PMID: 28218243