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Signals from the Gut Influence Mouse Behavior: Examination of Mechanisms
Author(s) -
Peterson Diana Coomes
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.511.1
Subject(s) - optogenetics , jejunum , halorhodopsin , neuroscience , vagus nerve , migrating motor complex , biology , biophysics , anatomy , small intestine , endocrinology , stimulation , biochemistry , bacteriorhodopsin , membrane
The intestinal microflora can have significant influences on brain activity. Gut microbiota release neurotransmitters that are hypothesized to send signals via the vagal nerve back to the brain. However, such afferent interactions have never been proven. The current experiments utilized optogenetic vectors (AAV‐CaMKIIa‐eNpHR3.0‐EYFP) placed within the jejunum to label vagal nerves. These vectors induce the insertion of light sensitive chloride channels into neuronal membranes that when stimulated with light deactivate the neuron. By placing these vectors in the jejunum, the experiment selectively deactivated only the select fibers that run from the jejunum to the brain. Control animals were injected with saline. In all animals, normal animal behavior was recorded for anxiety measures (elevated plus maze), open field behaviors, and forced swim tests. Each test was performed with both light deactivation of the vagus, and no‐light conditions. Results indicated that mouse behavior was not affected for the control animals nor for animals in the no‐light vector conditions. However, the animal behavior was dramatically altered for each animal in the optogenetic light deactivation condition. In each behavioral test, animals showed a freezing behavior for the extent of time that the vagus was deactivated. Within the forced swim experiments, frozen animals did not keep their head above water and tended to sink to the bottom of the tank (requiring multiple rescues during each session). The results support the hypothesis that the jejunum can influence brain activity via vagal nerve efferents. I conclude that optogenetic deactivation of the vagal afferents of the jejunum has a direct influence on animal behavior and thus brain circuits. Therefore, this pathway provides an optimal mechanism by which future nutritional therapies can be devised for a variety of brain pathologies. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .