The aim of this study was to determine the effect of streptokinase (SK) on the ultrastructure of cellular elements in the cerebral cortex of newborn rats in vitro. Three series of cell cultures grown on DMEM were used, including those grown on the medium enriched with 15% fetal calf serum (control 1), cultures transferred to the depleted medium containing only 0.5% of this serum (control 2), and the experimental cultures, to which SK (2000 IU/ml) was added. Addition of SK to the medium prevented a reduction of the viability of mature (14 days) dissociated neocortical cell culture from 1-2-day-old rats, induced by a transfer of the culture to a blood serum protein-deficient medium. In a 7-day culture SK potentiated the decrease in the cell viability. In organotypical cultures, with the use of electron microscopy, it was found that SK in concentration used prevented the development of destructive changes in astrocytes, oligodendrocytes, and neurons of explants, induced by a deficit in serum proteins. The neurons contained numerous mitochondria, some of which had only a few cristae. Signs of destruction were observed only in neuronal nuclei. After exposure to SK for 48 hours an activation of oligodendrocytes (containing numerous myelin bodies) was noted which was accompanied by astrocyte disintegration (with hyperchromatic nuclei in the remaining cells). The neurons were resistant to SK exposure.
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NPJ Parkinsons Dis
January 2025
Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, 20852, USA.
ΑBSTRACT: In Parkinson's disease (PD), Lewy pathology deposits in the cerebral cortex, but how the pathology disrupts cortical circuit integrity and function remains poorly understood. To begin to address this question, we injected α-synuclein (αSyn) preformed fibrils (PFFs) into the dorsolateral striatum of mice to seed αSyn pathology in the cortical cortex and induce degeneration of midbrain dopaminergic neurons. We reported that αSyn aggregates accumulate in the motor cortex in a layer- and cell-subtype-specific pattern.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Pharmacology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Cortical interneurons generated from ganglionic eminence via a long-distance journey of tangential migration display evident cellular and molecular differences across brain regions, which seeds the heterogeneous cortical circuitry in primates. However, whether such regional specifications in interneurons are intrinsically encoded or gained through interactions with the local milieu remains elusive. Here, we recruit 685,692 interneurons from cerebral cortex and subcortex including ganglionic eminence within the developing human and macaque species.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Intelligent Precision Healthcare Convergence, Sungkyunkwan University, Suwon, Republic of Korea.
Our naturalistic experiences are organized into memories through multiple processes, including novelty encoding, memory formation, and retrieval. However, the neural mechanisms coordinating these processes remain elusive. Using fMRI data acquired during movie viewing and subsequent narrative recall, we examine hippocampal neural subspaces associated with distinct memory processes and characterized their relationships.
View Article and Find Full Text PDFJ Neurosci
January 2025
Laboratory of Cerebral Cortex Research, HUN-REN Institute of Experimental Medicine, Budapest, Hungary
The human hippocampus, essential for learning and memory, is implicated in numerous neurological and psychiatric disorders, each linked to specific neuronal subpopulations. Advancing our understanding of hippocampal function requires computational models grounded in precise quantitative neuronal data. While extensive data exist on the neuronal composition and synaptic architecture of the rodent hippocampus, analogous quantitative data for the human hippocampus remain very limited.
View Article and Find Full Text PDFJ Psychiatry Neurosci
January 2025
From the Department of Psychiatry, Yale University School of Medicine, New Haven, Conn., USA (Chen, Luo, Ide, C.-S. Li); Yale University, New Haven, Conn., USA (H.-T. Li); the Department of Biomedical Engineering, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China (G. Li); the Beijing International Science and Technology Cooperation Base for Intelligent Physiological Measurement and Clinical Transformation, Beijing, China (G. Li); the Department of Neuroscience, Yale University School of Medicine, New Haven, Conn., USA (C.-S Li); the Interdepartment Neuroscience Program, Yale University, New Haven, Conn., USA (C.-S. Li); the Wu Tsai Institute, Yale University, New Haven, Conn., USA (C.-S. Li).
Background: Genetic variants may confer risk for depression by modulating brain structure and function; evidence has underscored the key role of the subgenual anterior cingulate cortex (sgACC) in depression. We sought to examine how the resting-state functional connectivity (rsFC) of the sgACC was associated with polygenic risk for depression in a subclinical population.
Methods: Following published protocols, we computed seed-based whole-brain sgACC rsFC and calculated polygenic risk scores (PRS) using data from healthy young adults from the Human Connectome Project.
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