98%
921
2 minutes
20
Probe electrospray ionization (PESI), which is an ambient ionization technique, enables us to analyze intact endogenous metabolites without sample preparation. In this study, we applied the newly developed method of PESI coupled to tandem mass spectrometry (PESI/MS/MS) to analyze metabolites in mouse brain, where its lipid composition often interfere with MS-based metabolome analysis. As a result, PESI/MS/MS directly detected 25 metabolites in a mouse frontal cortex, and clearly discriminated the metabolic profiles of mice model with energy metabolism disruption from control mice. PESI/MS/MS also allowed us to perform local distribution analysis of the hippocampus as well as the frontal cortex in each mouse (n = 5), discriminating their subtle metabolic differences. These results showed high potential of PESI/MS/MS for direct metabolome profiling of mouse brain.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.aca.2017.06.047 | 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.
View Article and Find Full Text PDFJ Virol
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.
View Article and Find Full Text PDF