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Objective: Resting-state functional connectivity (rsFC) of the human brain is closely related with neurological and psychiatric disorders. Mice are widely used to investigate the physiological mechanisms of such disorders, because of the applicability of invasive experimental techniques. Thus, studies on rsFC of the mouse brain are essential to link physiological mechanisms with these disorders in humans. In this study, we investigated the applicability of intrinsic optical signal imaging of cerebral blood volume (IOSI-CBV) for rsFC analysis of the mouse brain.
Approach: Transcranial IOSI-CBV images were collected from the brains of un-anesthetized wild-type mice with a cooled-CCD camera. The time traces of all pixels were averaged to create a global signal (GS). Marginal and partial correlation analyses were performed to estimate the rsFC based on CBV signals both with and without GS removal. The consistency of the results were confirmed by comparing them with to the rsFCs data reported in the previous studies.
Main Results: We confirmed that GS correlated with heart rate fluctuation in the FC frequency band. The marginal correlation coefficient of CBV with GS removal was consistent with measurements using conventional optical imaging methods relying on oxygenated hemoglobin concentration and cerebral blood flow.
Significance: These results suggest the applicability and usefulness of the transcranial IOSI-CBV method to estimate rsFC of the mouse brain.
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http://dx.doi.org/10.1088/1361-6579/aac033 | DOI Listing |
J Cell Biol
November 2025
Life Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Two major protein recycling pathways have emerged as key regulators of enduring forms of synaptic plasticity, such as long-term potentiation (LTP), yet how these pathways are recruited during plasticity is unknown. Phosphatidylinositol-3-phosphate (PI(3)P) is a key regulator of endosomal trafficking and alterations in this lipid have been linked to neurodegeneration. Here, using primary hippocampal neurons, we demonstrate dynamic PI(3)P synthesis during chemical induction of LTP (cLTP), which drives coordinate recruitment of the SNX17-Retriever and SNX27-Retromer pathways to endosomes and synaptic sites.
View Article and Find Full Text PDFBrain
September 2025
Central European Institute of Technology Masaryk University (CEITEC MU), 625 00 Brno, Czech Republic.
Mutations in the human ADAR gene encoding adenosine deaminase acting on RNA 1 (ADAR1) cause Aicardi-Goutières syndrome 6 (AGS6); a severe auto-inflammatory encephalopathy with aberrant interferon (IFN) induction. AdarΔ2-13 null mutant mouse embryos lacking ADAR1 protein die with high levels of IFN-stimulated gene (ISG) transcripts. In Adar Mavs double mutants also lacking the Mitochondrial antiviral signaling (MAVS) adaptor, the aberrant IFN induction is prevented.
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September 2025
Laboratory of Virology, Wageningen University & Research, Wageningen, the Netherlands.
Vertebrate animals and many small DNA and single-stranded RNA viruses that infect vertebrates have evolved to suppress genomic CpG dinucleotides. All organisms and most viruses additionally suppress UpA dinucleotides in protein-coding RNA. Synonymously recoding viral genomes to introduce CpG or UpA dinucleotides has emerged as an approach for viral attenuation and vaccine development.
View Article and Find Full Text PDFEur J Neurosci
September 2025
Department of Anesthesiology and Pain Medicine, University of California Davis, Davis, California, USA.
Voltage-gated K channels of the Kv2 family coassemble with electrically silent KvS subunits in specific subpopulations of brain neurons, forming heteromeric Kv2/KvS channels with distinct functional properties. Little is known about the composition and function of Kv2 channels in spinal cord neurons, however. Here, we show that while Kv2.
View Article and Find Full Text PDFJ Virol
September 2025
Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur, West Bengal, India.
High morbidity and mortality associated with human β-coronavirus (CoV) infection highlight the need to determine host responses to infection and develop anti-viral therapies. Gap junction intercellular communication (GJIC), particularly involving Connexin43 (Cx43), is vital for maintaining central nervous system (CNS) homeostasis, and disruption of GJIC is a well-documented pathogenic mechanism among β-coronaviruses. Specifically, murine β-coronavirus, mouse hepatitis virus (MHV-A59) inoculation in the mouse brain causes acute-stage CNS viral spread and chronic neuroinflammatory demyelination while causing pronounced downregulation of Cx43 at the acute stage, reflecting a critical role in CNS pathology.
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