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德尔塔阿片受体介导海马 CA2 区表达钙结合蛋白的中间神经元的独特可塑性。

Delta-opioid receptors mediate unique plasticity onto parvalbumin-expressing interneurons in area CA2 of the hippocampus.

机构信息

Université Paris Descartes, Sorbonne Paris Cité, IFR 95, CNRS UMR8118, Equipe ATIP, 75006 Paris, France.

出版信息

J Neurosci. 2013 Sep 4;33(36):14567-78. doi: 10.1523/JNEUROSCI.0649-13.2013.

Abstract

Inhibition is critical for controlling information transfer in the brain. However, the understanding of the plasticity and particular function of different interneuron subtypes is just emerging. Using acute hippocampal slices prepared from adult mice, we report that in area CA2 of the hippocampus, a powerful inhibitory transmission is acting as a gate to prevent CA3 inputs from driving CA2 neurons. Furthermore, this inhibition is highly plastic, and undergoes a long-term depression following high-frequency 10 Hz or theta-burst induction protocols. We describe a novel form of long-term depression at parvalbumin-expressing (PV+) interneuron synapses that is dependent on delta-opioid receptor (DOR) activation. Additionally, PV+ interneuron transmission is persistently depressed by DOR activation in area CA2 but only transiently depressed in area CA1. These results provide evidence for a differential temporal modulation of PV+ synapses between two adjacent cortical circuits, and highlight a new function of PV+ cells in controlling information transfer.

摘要

抑制对于控制大脑中的信息传递至关重要。然而,对于不同中间神经元亚型的可塑性和特定功能的理解才刚刚开始。我们使用从成年小鼠制备的急性海马切片报告说,在海马体的 CA2 区域,强大的抑制性传递充当了一个门,以防止 CA3 输入驱动 CA2 神经元。此外,这种抑制具有高度的可塑性,并且在高频 10 Hz 或θ爆发诱导方案后会经历长时程抑制。我们描述了一种新型的长时程抑制在表达囊泡相关蛋白(PV+)的中间神经元突触上,该抑制依赖于δ-阿片受体(DOR)的激活。此外,DOR 在 CA2 区的激活会持续抑制 PV+神经元的传递,但在 CA1 区只会短暂抑制。这些结果为两个相邻皮质回路中 PV+突触的差异时间调制提供了证据,并突出了 PV+细胞在控制信息传递中的新功能。

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