Gut vagal sensory signaling regulates hippocampus function through multi-order pathways.

Gut vagal sensory signaling regulates hippocampus function through multi-order pathways.
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DOI:
10.1038/s41467-018-04639-1
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发表时间:
2018-06-05
影响因子:
16.6
通讯作者:
Kanoski SE
Kanoski SE
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Suarez AN;Hsu TM;Liu CM;Noble EE;Cortella AM;Nakamoto EM;Hahn JD;de Lartigue G;Kanoski SE

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迷走神经是胃肠(GI)道和大脑之间神经通讯的主要方式。迷走神经介导的GI信号激活海马体(HPC),这是一个经典的与记忆功能相关的大脑区域。然而,GI衍生的迷走HPC通信的内源性相关性尚不清楚。在这里,我们利用皂草素(SAP)为基础的损伤程序,以揭示大鼠的选择性GI迷走神经感觉/传入消融损害HPC依赖的情节和空间记忆,与减少HPC神经营养和神经发生标志物的影响。为了确定连接肠道到HPC的神经通路,我们利用基于单突触和多突触病毒的追踪方法来识别内侧隔作为连接内侧孤束核(GI迷走神经传入突触)到背侧HPC神经元的中继。我们的结论是,内源性GI衍生的迷走神经感觉信号促进HPC依赖的记忆功能,通过多级脑干间隔通路,从而确定了以前未知的作用,肠-脑轴的记忆控制。进食相关的迷走神经信号发生在胃肠道和大脑之间,但目前还不清楚这种途径是否会影响认知过程。这项研究表明,内源性胃肠道源性迷走神经感觉信号通过多级脑干-隔通路促进海马依赖性记忆功能。
The vagus nerve is the primary means of neural communication between the gastrointestinal (GI) tract and the brain. Vagally mediated GI signals activate the hippocampus (HPC), a brain region classically linked with memory function. However, the endogenous relevance of GI-derived vagal HPC communication is unknown. Here we utilize a saporin (SAP)-based lesioning procedure to reveal that selective GI vagal sensory/afferent ablation in rats impairs HPC-dependent episodic and spatial memory, effects associated with reduced HPC neurotrophic and neurogenesis markers. To determine the neural pathways connecting the gut to the HPC, we utilize monosynaptic and multisynaptic virus-based tracing methods to identify the medial septum as a relay connecting the medial nucleus tractus solitarius (where GI vagal afferents synapse) to dorsal HPC glutamatergic neurons. We conclude that endogenous GI-derived vagal sensory signaling promotes HPC-dependent memory function via a multi-order brainstem–septal pathway, thereby identifying a previously unknown role for the gut–brain axis in memory control. Feeding-relevant vagal signaling occurs between the gastrointestinal tract and the brain, but it is unclear if this pathway influences cognitive processes. This study shows that endogenous gastrointestinal derived vagal sensory signaling promotes hippocampal-dependent memory function via a multi-order brainstem–septal pathway.
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