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Immature neurons undergo morphological and physiological maturation in order to establish neuronal networks. During neuronal maturation, a large number of genes change their transcriptional levels, and these changes may be mediated by chromatin modifiers. In this study, we found that the level of Ezh1, a component of Polycomb repressive complex 2 (PRC2), increases during neuronal maturation in mouse neocortical culture. In addition, conditional knockout of Ezh1 in post-mitotic excitatory neurons leads to downregulation of a set of genes related to neuronal maturation. Moreover, the locus encoding Cpg15/Neuritin (Nrn1), which is regulated by neuronal activity and implicated in stabilization and maturation of excitatory synapses, is a direct target of Ezh1 in cortical neurons. Together, these results suggest that elevated expression of Ezh1 contributes to maturation of cortical neurons.
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http://dx.doi.org/10.5582/ddt.2021.01017 | DOI Listing |
J Comput Neurosci
September 2025
School of Electrical and Information Engineering, Tianjin University, Tianjin, 300072, China.
Transcranial alternating current stimulation (tACS) enables non-invasive modulation of brain activity, holding promise for cognitive research and clinical applications. However, it remains unclear how the spiking activity of cortical neurons is modulated by specific electric field (E-field) distributions. Here, we use a multi-scale computational framework that integrates an anatomically accurate head model with morphologically realistic neuron models to simulate the responses of layer 5 pyramidal cells (L5 PCs) to the E-fields generated by conventional M1-SO tACS.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Department of Pharmacology, Govt. College of Pharmacy, Rohru, Shimla, Himachal Pradesh, 171207, India.
Alzheimer's disease (AD) is the most common, complex, and untreatable form of dementia which is characterized by severe cognitive, motor, neuropsychiatric, and behavioural impairments. These symptoms severely reduce the quality of life for patients and impose a significant burden on caregivers. The existing therapies offer only symptomatic relief without addressing the underlying silent pathological progression.
View Article and Find Full Text PDFMol Psychiatry
September 2025
Department of Physiology and Biophysics, State University of New York at Buffalo, Buffalo, NY, 14203, US.
Hyperphosphorylation of Tau and the ensuing microtubule destabilization are linked to synaptic dysfunction in Alzheimer's disease (AD). We find a marked increase of phosphorylated Tau (pTau) in cortical neurons differentiated from induced pluripotent stem cells (iPSCs) of AD patients. It is accompanied by significantly elevated expression of Serum and Glucocorticoid-regulated Kinase-1 (SGK1), which is induced by cellular stress, and Histone Deacetylase 6 (HDAC6), which deacetylates tubulin to destabilize microtubules.
View Article and Find Full Text PDFNeuropsychopharmacology
September 2025
Neuroscience Center, HiLIFE, University of Helsinki, Helsinki, Finland.
Chronic treatment with fluoxetine, a widely prescribed selective serotonin reuptake inhibitor (SSRI), is known to promote neural plasticity. The role of fluoxetine in plasticity has been particularly tied to parvalbumin-positive interneurons, a key population of GABAergic neurons that regulate inhibitory tone and network stability. While our previous studies have highlighted fluoxetine-induced plasticity in the visual cortex and hippocampus, its cell-type-specific effects in the prefrontal cortex (PFC) remain unclear.
View Article and Find Full Text PDFNeuroimage
September 2025
Danish Research Centre for Magnetic Resonance, Department of Radiology and Nuclear Medicine, Copenhagen University Hospital - Amager and Hvidovre, Copenhagen, Denmark, Kettegård Allé 30, 2650 Hvidovre, Denmark; Institute of Neuroscience, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N,
Background: We recently demonstrated that single-pulse TMS of the primary sensorimotor hand area (SM1) elicits an immediate transcranial evoked potential (iTEP). This iTEP response appears within 2-8 ms post-TMS, featuring high-frequency peaks superimposed on a slow positive wave. Here, we used a linear TMS-EEG mapping approach to characterize the rostro-caudal iTEP expression and compared it to that of motor-evoked potentials (MEPs).
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