Highlights
- •A comprehensive global evaluation of the hippocampal monoamine neurotransmitters in germ-free (GF) mice.
- •Absence of gut microbiota markedly affects hippocampal monoamine genes, impairing the development of brain and behaviors.
- •Altered anxiolytic behaviors and monoamine genes induced by GF status could't be reversed by colonization at adolescence.
Abstract
The gut microbiome is composed of an enormous number of microorganisms, generally
regarded as commensal bacteria. Resident gut bacteria are an important contributor
to health and significant evidence suggests that the presence of healthy and diverse
gut microbiota is important for normal cognitive and emotional processing. Here we
measured the expression of monoamine neurotransmitter-related genes in the hippocampus
of germ-free (GF) mice and specific-pathogen-free (SPF) mice to explore the effect
of gut microbiota on hippocampal monoamine functioning. In total, 19 differential
expressed genes (Htr7, Htr1f, Htr3b, Drd3, Ddc, Maob, Tdo2, Fos, Creb1, Akt1, Gsk3a,
Pik3ca, Pla2g5, Cyp2d22, Grk6, Ephb1, Slc18a1, Nr4a1, Gdnf) that could discriminate
between the two groups were identified. Interestingly, GF mice displayed anxiolytic-like
behavior compared to SPF mice, which were not reversed by colonization with gut microbiota
from SPF mice. Besides, colonization of adolescent GF mice by gut microbiota was not
sufficient to reverse the altered gene expression associated with their GF status.
Taking these findings together, the absence of commensal microbiota during early life
markedly affects hippocampal monoamine gene-regulation, which was associated with
anxiolytic behaviors and monoamine neurological signs.
Keywords
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Article info
Publication history
Published online: March 29, 2019
Accepted:
March 28,
2019
Received in revised form:
February 17,
2019
Received:
July 30,
2018
Identification
Copyright
© 2019 Published by Elsevier B.V.