The idea of self-organized signal processing in the cerebral cortex has become a focus of research since Beggs and Plentz reported avalanches in local field potential recordings from organotypic cultures and acute slices of rat somatosensory cortex. How the cortex intrinsically organizes signals remains unknown. A current hypothesis was proposed by the condensed matter physicists Bak, Tang, and Wiesenfeld when they conjectured that if neuronal avalanche activity followed inverse power law distributions, then brain activity may be set around phase transitions within self-organized signals. We asked if we would observe self-organized signals in an isolated slice of our data driven detailed simulation of the mouse primary motor cortex? If we did, would we observe avalanches with power-law distributions in size and duration and what would they look like? Our results demonstrate that a brief unstructured stimulus (100ms, 57 A current) to a small subset of neurons (about 181 of more than 10,000) in a simulated mouse primary motor cortex slice results in self-organized and self-sustained avalanches with power-law size and duration distributions and values similar to those reported from in vivo and in vitro experiments. We observed 4 cross-layer and cross-neuron population patterns, 3 of which displayed a dominant rhythmic component. Avalanches were each composed of one or more of the 4 population patterns.
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http://dx.doi.org/10.1101/2025.01.13.632866 | DOI Listing |
Stem Cell Res Ther
January 2025
College & Hospital of Stomatology, Key Laboratory of Oral Diseases Research of Anhui Province, Anhui Medical University, Hefei, 230032, China.
Background: The aging of bone marrow mesenchymal stem cells (BMSCs) impairs bone tissue regeneration, contributing to skeletal disorders. LncRNA NEAT1 is considered as a proliferative inhibitory role during cellular senescence, but the relevant mechanisms remain insufficient. This study aims to elucidate how NEAT1 regulates mitotic proteins during BMSCs aging.
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Neurology, Division of Neuroimmunology, School of Medicine, Johns Hopkins University, Baltimore, MD, 21287, USA.
Chronic innate immune activation in the central nervous system (CNS) significantly contributes to neurodegeneration in progressive multiple sclerosis (MS). Using multiple experimental autoimmune encephalomyelitis (EAE) models, we discovered that NLRX1 protects neurons in the anterior visual pathway from inflammatory neurodegeneration. We quantified retinal ganglion cell (RGC) density and optic nerve axonal degeneration, gliosis, and T-cell infiltration in Nlrx1 and wild-type (WT) EAE mice and found increased RGC loss and axonal injury in Nlrx1 mice compared to WT mice in both active immunization EAE and spontaneous opticospinal encephalomyelitis (OSE) models.
View Article and Find Full Text PDFMol Psychiatry
January 2025
Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA.
Age-related dopamine (DA) neuron loss is a primary feature of Parkinson's disease. However, whether similar biological processes occur during healthy aging, but to a lesser degree, remains unclear. We therefore determined whether midbrain DA neurons degenerate during aging in mice and humans.
View Article and Find Full Text PDFCell Signal
January 2025
Department of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, Taiyuan 030001, China. Electronic address:
Hepatic stellate cells (HSCs) are the central link of the occurrence and development of hepatic fibrosis, and autophagy promotes HSCs activation. N6-methyladenosine (m6A) RNA modification can also control autophagy by targeting selected autophagy-associated genes. but up to now, little research has been done on the m6A modification autophagy-related genes (ATGs) in hepatic fibrosis.
View Article and Find Full Text PDFNeurobiol Dis
January 2025
Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, University of Saskatchewan, Saskatoon, SK S7K 0M7, Canada; Neurology Division, Department of Medicine, University of Saskatchewan, Saskatoon, SK S7N 0X8, Canada. Electronic address:
RNA binding protein dysfunction is a pathogenic feature of multiple neurological diseases, including multiple sclerosis (MS). Neurodegeneration (the loss of, or damage to neurons and axons) is the primary driver of disease progression in MS. Herein, we utilized a novel, neuron-specific model of neurodegeneration by transducing primary mouse neurons with mutant forms of the RNA binding protein heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) identified from MS patients, including one within the M9-nuclear localization sequence of hnRNP A1 (A1(P275S)) and a second in the prion-like domain of hnRNP A1 (A1(F263S)) to test the hypothesis that neuronal hnRNP A1 dysfunction drives neurodegeneration in MS.
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