The gut metabolite indole-3-propionic acid activates ERK1 to restore social function and hippocampal inhibitory synaptic transmission in a 16p11.2 microdeletion mouse model - Jiang, Jian; Wang, Dilong; Jiang, Youheng; Yang, Xiuyan; Sun, Runfeng; Chang, Jinlong; Zhu, Wenhui; Yao, Peijia; Song, Kun; Chang, Shuwen; Wang, Hong; Zhou, Lei; et al. (Microbiome, 2024)
Keywords: Animals; Autism; Autism Spectrum Disorder; Behavior; Bioinformatics; Biomedical and Life Sciences; Biomedicine; Blood circulation; Chromosome 16; Cognitive ability; Dentate gyrus; Dysbacteriosis; Feces; GABA; Genes; Genetic aspects; Genetic transcription; Genetic translation; Gut microbiota metabolite; Gut-brain axis; Health aspects; Health maintenance organizations; Hippocampus; Humans; Indole-3-propionic acid; Indoles; Intestinal microflora; Mapk3; Medical Microbiology; Memory; Metabolism; Metabolites; Mice; Microbial Ecology; Microbial Genetics and Genomics; Microbiology; Microbiota; Microbiota (Symbiotic organisms); Molecular modelling; Nervous system; Neurodevelopmental disorders; Neurons; Oral administration; Pathogenesis; Phenotypes; Phosphorylation; Preferences; Propionates; Propionic acid; Recovery of function; Social deficits; Synaptic Transmission; Virology; China; Indole-3-propionic acid; GABA; Autism; Social deficits; Gut microbiota metabolite; Mapk3