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Protocol for investigating astrocytic mitochondria in neurons of adult mice using two-photon microscopy.
STAR Protoc
January 2025
Department of Neurosurgery, the First Affiliated Hospital of Jinan University, Guangzhou, China; Department of Neurosurgery, the Affiliated Hospital, Southwest Medical University, Luzhou 646000, China; Laboratory of Neurological Diseases and Brain Function, the Affiliated Hospital, Southwest Medical University, Luzhou 646000, China. Electronic address:
Under pathological conditions, astrocytes can transfer mitochondria to neurons, where they exert neuroprotective effects. In this context, we present a protocol for capturing astrocytic mitochondria in neurons of adult mice using a two-photon microscope. We describe an approach for constructing a mouse model with combined labeling of astrocytic mitochondria and neurons.
View Article and Find Full Text PDFMitochondria as a Therapeutic Target: Focusing on Traumatic Brain Injury.
J Integr Neurosci
January 2025
Department of Hepatology, Federal University of Health Sciences of Porto Alegre (UFCSPA), 90050-170 Porto Alegre, Rio Grande do Sul (RS), Brazil.
Mitochondria are organelles of eukaryotic cells delimited by two membranes and cristae that consume oxygen to produce adenosine triphosphate (ATP), and are involved in the synthesis of vital metabolites, calcium homeostasis, and cell death mechanisms. Strikingly, normal mitochondria function as an integration center between multiple conditions that determine neural cell homeostasis, whereas lesions that lead to mitochondrial dysfunction can desynchronize cellular functions, thus contributing to the pathophysiology of traumatic brain injury (TBI). In addition, TBI leads to impaired coupling of the mitochondrial electron transport system with oxidative phosphorylation that provides most of the energy needed to maintain vital functions, ionic homeostasis, and membrane potentials.
View Article and Find Full Text PDFDe Novo Pathogenic Variant Associated with Lethal Encephalocardiomyopathy-Case Report and Literature Review.
Int J Mol Sci
January 2025
Institute for Maternal and Child Health IRCCS Burlo Garofolo, Via dell'Istria, 65, 34137 Trieste, Italy.
Pathogenic variants in , encoding dynamin-like protein-1 (DRP1), cause a lethal encephalopathy. DRP1 defective function results in altered mitochondrial networks, characterized by elongated/spaghetti-like, highly interconnected mitochondria. We validated in yeast the pathogenicity of a de novo variant identified by whole exome sequencing performed more than 10 years after the patient's death.
View Article and Find Full Text PDFUltrastructural Study and Immunohistochemical Characteristics of Mesencephalic Tegmentum in Juvenile Chum Salmon () Brain After Acute Traumatic Injury.
Int J Mol Sci
January 2025
A.V. Zhirmunsky National Scientific Center of Marine Biology, Far Eastern Branch, Russian Academy of Sciences, 690041 Vladivostok, Russia.
The ultrastructural organization of the nuclei of the tegmental region in juvenile chum salmon () was examined using transmission electron microscopy (TEM). The dorsal tegmental nuclei (DTN), the nucleus of (NFLM), and the nucleus of the oculomotor nerve (NIII) were studied. The ultrastructural examination provided detailed ultrastructural characteristics of neurons forming the tegmental nuclei and showed neuro-glial relationships in them.
View Article and Find Full Text PDFVDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration.
Biomolecules
December 2024
Department of Physiology and Cell Biology, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 84105, Israel.
Voltage-Dependent Anion Channel 1 (VDAC1) is a mitochondrial outer membrane protein that plays a crucial role in regulating cellular energy metabolism and apoptosis by mediating the exchange of ions and metabolites between mitochondria and the cytosol. Mitochondrial dysfunction and oxidative stress are central features of neurodegenerative diseases. The pivotal functions of VDAC1 in controlling mitochondrial membrane permeability, regulating calcium balance, and facilitating programmed cell death pathways, position it as a key determinant in the delicate balance between neuronal viability and degeneration.
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