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Published on: January 7, 2019
Gut vagal sensory signaling regulates hippocampus function through multi-order pathways
Andrea N Suarez1, Ted M Hsu2,3, Clarissa M Liu1,2
1Human and Evolutionary Biology Section, Department of Biological Sciences, University of Southern California, Los Angeles, California, USA.
Gut signals via the vagus nerve are crucial for memory. Disrupting this gut-brain axis impairs hippocampus-dependent memory and reduces brain markers of neurogenesis, revealing a new role for gut-brain communication in memory control.
Area of Science:
- Neuroscience
- Gastroenterology
- Psychology
Background:
- The vagus nerve facilitates neural communication between the gastrointestinal (GI) tract and the brain.
- GI signals transmitted via the vagus nerve activate the hippocampus (HPC), a region vital for memory.
- The endogenous role of this GI-vagal-HPC communication in memory remains unclear.
Purpose of the Study:
- To investigate the functional relevance of GI-derived vagal sensory signals in HPC-dependent memory.
- To elucidate the neural pathways mediating gut-to-HPC communication.
Main Methods:
- Selective ablation of GI vagal afferents using saporin (SAP) lesions in rats.
- Assessment of HPC-dependent episodic and spatial memory.
- Measurement of HPC neurotrophic and neurogenesis markers.
- Viral tracing (monosynaptic and multisynaptic) to map neural circuitry.
Main Results:
- GI vagal sensory denervation significantly impaired episodic and spatial memory in rats.
- Lesioned rats exhibited reduced hippocampal neurotrophic and neurogenesis markers.
- Neural tracing identified the medial septum as a key relay in the brainstem-septal pathway connecting the GI tract to the dorsal HPC.
Conclusions:
- Endogenous GI-derived vagal sensory signaling is essential for optimal HPC-dependent memory function.
- A multi-order brainstem-septal pathway mediates this gut-brain communication.
- This study reveals a novel role for the gut-brain axis in regulating memory processes.
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