Université de Bordeaux, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33076 Bordeaux, France.
Centre National de la Recherche Scientifique, Interdisciplinary Institute for Neuroscience, UMR 5297, F-33076 Bordeaux, France.
Nat Commun. 2017 Feb 20;8:14456. doi: 10.1038/ncomms14456.
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.
焦虑受多个神经元回路控制，这些回路与终纹床核（BNST）之间存在强大且相互的联系，BNST 是控制负面情绪状态的关键结构。然而，BNST 如何整合多种输入来调节焦虑仍然未知。在这项研究中，我们评估了边缘前皮质（ILCx）和腹侧下托/CA1（vSUB/CA1）输入在调节 BNST 活动方面的贡献，使用从单个电穿孔神经元的突触传递和体内记录，我们表明 vSUB/CA1 刺激在 BNST 的前内侧部分（amBNST）在单细胞水平上促进相反形式的体内可塑性。我们发现 NMDA 受体依赖性的同突触长时程增强对于抗焦虑作用至关重要。这些发现表明，amBNST 中的 vSUB/CA1 驱动的 LTP 参与引发对焦虑环境的适当反应，而这种补偿机制的功能障碍可能是病理性焦虑状态的基础。
