The gut microbes perform several beneficial functions which impact the periphery and central nervous systems of the host. Gut microbiota dysbiosis is acknowledged as a major contributor to the development of several neuropsychiatric and neurological disorders including bipolar disorder, depression, anxiety, Parkinson's disease, Alzheimer's disease, attention deficit hyperactivity disorder, and autism spectrum disorder. Thus, elucidation of how the gut microbiota-brain axis plays a role in health and disease conditions is a potential novel approach to prevent and treat brain disorders. The zebrafish () is an invaluable vertebrate model that possesses conserved brain and intestinal features with those of humans, thus making zebrafish a valued model to investigate the interplay between the gut microbiota and host health. This chapter describes current findings on the utility of zebrafish in understanding molecular mechanisms of neurotoxicity mediated via the gut microbiota-brain axis. Specifically, it highlights the utility of zebrafish as a model organism for understanding how anthropogenic chemicals, pharmaceuticals and bacteria exposure affect animals and human health via the gut-brain axis.
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http://dx.doi.org/10.1016/bs.ant.2024.02.003 | DOI Listing |
Curr Opin Neurobiol
December 2024
Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO 63110, USA; Department of Developmental Biology, Washington University School of Medicine, Saint Louis, MO 63110, USA; Brain Immunology and Glia Center, Washington University School of Medicine, Saint Louis, MO 63110, USA. Electronic address:
Critical periods are brief windows of heightened neural circuit plasticity that allow circuits to permanently reset their structure and function to facilitate robust organismal behavior. Understanding the cellular and molecular mechanisms that instruct critical period timing is of broad clinical interest, as altered developmental plasticity is linked to multiple neurodevelopmental disorders. While intrinsic, neuronal mechanisms shape both neural circuit remodeling and critical period timing, recent data indicate that signaling from astrocytes and surrounding glia can both promote and limit critical period plasticity.
View Article and Find Full Text PDFJ Neurochem
January 2025
Division of Molecular Neuroimmunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Stress is a significant cause of mental disorders, for which effective treatments remain limited due to an insufficient understanding of its pathogenic mechanisms. Recent research has increasingly focused on non-neuronal cells to elucidate the molecular mechanisms underlying psychopathology. In this review, we summarize the current knowledge on how non-neuronal cells in the central nervous system, including microglia, astrocytes, and oligodendrocytes, respond to peripherally derived stress-related factors and how these responses contribute to the development of mental disorders.
View Article and Find Full Text PDFDiscov Oncol
December 2024
Department of Radiotherapy, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221000, China.
High expression of immune checkpoint molecule B7-H3 (CD276) in many cancer types makes it a promising immunotherapeutic target. Both coinhibitory and costimulatory effects of B7-H3 in tumors have been demonstrated, but the mechanism of B7-H3 immune response under dual effects is open to question. B7-H3 is crucially involved in the migration and invasion, angiogenesis, metabolism and chemotherapy resistance of prostate cancer.
View Article and Find Full Text PDFPlant Mol Biol
December 2024
State Key Laboratory of Crop Genetics & Germplasm Enhancement and Utilization, Zhongshan Biological Breeding laboratoryr, Nanjing Agricultural University, Nanjing, 210095, China.
J Physiol
December 2024
Department of Biochemistry & Molecular Biology, University of Chicago, Chicago, IL, USA.
Volume-regulated anion channels (VRACs) are heteromeric complexes formed by proteins of the leucine-rich repeat-containing 8 (LRRC8) family. LRRC8A (also known as SWELL1) is the core subunit required for VRAC function, and it must combine with one or more of the other paralogues (i.e.
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