Proliferation and differentiation are tightly controlled during neural development. In the embryonic neural plate, primary neurogenesis is driven by the proneural pathway. Here we report the characterization of Maturin, a novel, evolutionarily conserved protein that is required for normal primary neurogenesis. Maturin is detected throughout the early nervous system, yet it is most strongly expressed in differentiating neurons of the embryonic fish, frog and mouse nervous systems. Maturin expression can be induced by the proneural transcription factors Neurog2, Neurod1, and Ebf3. Maturin overexpression promotes neurogenesis, while loss-of-function inhibits the differentiation of neuronal progenitors, resulting in neural plate expansion. Maturin knockdown blocks the ability of Neurog2, Neurod1, and Ebf3 to drive ectopic neurogenesis. Maturin and Pak3, are both required for, and can synergize to promote differentiation of the primary neurons in vivo. Together, our results suggest that Maturin functions during primary neurogenesis and is required for the proneural pathway to regulate neural differentiation.
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http://dx.doi.org/10.1016/j.ydbio.2013.09.028 | DOI Listing |
J Cereb Blood Flow Metab
January 2025
Departments of Neurology and Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, USA.
Therapeutic drug development for central nervous system injuries, such as traumatic brain injury (TBI), presents significant challenges. TBI results in primary mechanical damage followed by secondary injury, leading to cognitive dysfunction and memory loss. Our recent study demonstrated the potential of carbon monoxide-releasing molecules (CORMs) to improve TBI recovery by enhancing neurogenesis.
View Article and Find Full Text PDFCells
January 2025
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Science, Moscow 117485, Russia.
Traumatic brain injury (TBI) is one of the major causes of severe neurological disorders and long-term dysfunction in the nervous system. Besides inducing neurodegeneration, TBI alters stem cell activity and neurogenesis within primary neurogenic niches. However, the fate of dividing cells in other brain regions remains unclear despite offering potential targets for therapeutic intervention.
View Article and Find Full Text PDFIBRO Neurosci Rep
June 2025
Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Oyo State, Nigeria.
From preclinical and clinical findings, it has been shown that the amygdala is a critical mediator of stress and primary target for stress effects in the brain. We investigated the neuroprotective effect of Ginkgolide B (GB) in repeated restraint stress-induced behavioral deficit and amygdalar inflammation in mice. Mice were orally pre-treated with GB 20 mg/kg 1 h prior to 4 h restraint stress for 21 consecutive days.
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January 2025
Department of Developmental and Regenerative Neurobiology, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
In the ventricular-subventricular-zone (V-SVZ) of the postnatal mammalian brain, immature neurons (neuroblasts) are generated from neural stem cells throughout their lifetime. These V-SVZ-derived neuroblasts normally migrate to the olfactory bulb through the rostral migratory stream, differentiate into interneurons, and are integrated into the preexisting olfactory circuit. When the brain is injured, some neuroblasts initiate migration toward the lesion and attempt to repair the damaged neuronal circuitry, but their low regeneration efficiency prevents functional recovery.
View Article and Find Full Text PDFPsychoradiology
December 2024
Department of Neurology, the First Hospital of Anhui Medical University, Hefei 230022, China.
Background: The hippocampus has been widely reported to be involved in the neuropathology of major depressive disorder (MDD). All the previous researches adopted group-level hippocampus subregions atlas to investigate abnormal functional connectivities in MDD in absence of capturing individual variability. In addition, the molecular basis of functional impairments of hippocampal subregions in MDD remains elusive.
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