This article comprehensively reviews how cerebral hypoxia impacts the physiological state of neurons and dendritic spines through a series of molecular changes, and explores the causal relationship between these changes and neuronal functional impairment. As a severe pathological condition, cerebral hypoxia can significantly alter the morphology and function of neurons and dendritic spines. Specifically, dendritic spines, being the critical structures for neurons to receive information, undergo changes such as a reduction in number and morphological abnormalities under hypoxic conditions. These alterations further affect synaptic function, leading to neurotransmission disorders. This article delves into the roles of molecular pathways like MAPK, AMPA receptors, NMDA receptors, and BDNF in the hypoxia-induced changes in neurons and dendritic spines, and outlines current treatment strategies. Neurons are particularly sensitive to cerebral hypoxia, with their apical dendrites being vulnerable to damage, thereby affecting cognitive function. Additionally, astrocytes and microglia play an indispensable role in protecting neuronal and synaptic structures, regulating their normal functions, and contributing to the repair process following injury. These studies not only contribute to understanding the pathogenesis of related neurological diseases but also provide important insights for developing novel therapeutic strategies. Future research should further focus on the dynamic changes in neurons and dendritic spines under hypoxic conditions and their intrinsic connections with cognitive function.
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http://dx.doi.org/10.1007/s10571-024-01491-4 | DOI Listing |
The effect of Constraint-induced movement therapy (CIMT) or Intermittent theta-burst stimulation (iTBS) alone is limited in improving motor function after a stroke. In this study, we explored the efficacy and possible mechanisms in combination of CIMT and iTBS through behavioral evaluation, RNA sequencing, Golgi staining, transmission electronic microscope (TEM), high-performance liquid chromatography (HPLC), western blotting (WB) and immunofluorescence. Firstly, we observed that combination therapy is safe and effective, and it can significantly reduce the number of immature dendritic spines and increase the number of functional dendritic spines, the amount of glutamate (Glu) and the expression of Glu1 receptor (Glu1R).
View Article and Find Full Text PDFPLoS Comput Biol
January 2025
Edmond and Lily Safra Center for Brain Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
Theoretical neuroscientists and machine learning researchers have proposed a variety of learning rules to enable artificial neural networks to effectively perform both supervised and unsupervised learning tasks. It is not always clear, however, how these theoretically-derived rules relate to biological mechanisms of plasticity in the brain, or how these different rules might be mechanistically implemented in different contexts and brain regions. This study shows that the calcium control hypothesis, which relates synaptic plasticity in the brain to the calcium concentration ([Ca2+]) in dendritic spines, can produce a diverse array of learning rules.
View Article and Find Full Text PDFPLoS One
January 2025
Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia, Canada.
Adult neurogenesis has most often been studied in the hippocampus and subventricular zone-olfactory bulb, where newborn neurons contribute to a variety of behaviors. A handful of studies have also investigated adult neurogenesis in other brain regions, but relatively little is known about the properties of neurons added to non-canonical areas. One such region is the striatum.
View Article and Find Full Text PDFJ Physiol
January 2025
Department of Physiology & Biomedical Engineering, Mayo Clinic, Rochester, MN, USA.
Motor neurons (MNs) within the nucleus ambiguus innervate the skeletal muscles of the larynx, pharynx and oesophagus, which are essential for swallow. Disordered swallow (dysphagia) is a serious problem in elderly humans, increasing the risk of aspiration, a key contributor to mortality. Despite this importance, very little is known about the pathophysiology of ageing dysphagia and the relative importance of frank muscle weakness compared to timing/activation abnormalities.
View Article and Find Full Text PDFCell Rep
January 2025
Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA; The Brain Tumor Center, Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:
Mutation or deletion of the deubiquitinase USP7 causes Hao-Fountain syndrome (HAFOUS), which is characterized by speech delay, intellectual disability, and aggressive behavior and highlights important unknown roles of USP7 in the nervous system. Here, we conditionally delete USP7 in glutamatergic neurons in the mouse forebrain, triggering disease-relevant phenotypes, including sensorimotor deficits, impaired cognition, and aggressive behavior. Although USP7 deletion induces p53-dependent neuronal apoptosis, most behavioral abnormalities in USP7 conditional knockout mice persist following p53 loss.
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