Objective: Genetic Absence Epilepsy Rat from Strasbourg (GAERS), a rodent model genetically predisposed to absence epilepsy, serves as an experimental tool to elucidate the neuronal mechanisms underlying human absence epilepsy. This study aimed to investigate the morphological features of dendrites and dendritic spines of pyramidal neurons in somatosensory cortex and hippocampus of Wistar and GAERS rats.
Material And Method: Adult male GAERS (n = 5) and control Wistar (n = 5) rats were sacrificed by transcardial perfusion and brains were removed. Brain tissues were processed by Golgi impregnation method using FD Rapid GolgiStain Kit. Coronal sections were obtained with a cryostat. Pyramidal neurons in layers V-VI of the somatosensory cortex and the CA1 region of the hippocampus were examined using a light microscope and Neurolucida 360 software. Dendrite nodes, dendrite segments (dendritic branching), dendrite terminations, total dendrite length, dendritic spine density, and dendritic spine types were analyzed.
Results: Compared to Wistar, GAERS exhibited significantly higher numbers of nodes (p = 0.0053, p = 0.0047), segments (p = 0.0036, p = 0.0036), and terminations (p = 0.0033, p = 0.0029) in the dendrites of the somatosensory cortex and the hippocampus, respectively. Furthermore, the total dendrite length (µm) (p = 0.0002, p = 0.0007) and the density of dendritic spines (1/µm) (p = 0.0168, p = 0.0120) were significantly high in GAERS compared to Wistar. When dendritic spine types were evaluated separately, stubby-type dendritic spines in the hippocampus were higher in GAERS compared to Wistar (p = 0.0045).
Conclusion: Intense synaptic connections in the somatosensory cortex and the hippocampus of genetic absence epileptic rats led to morphological alterations in the dendrites and the dendritic spines of pyramidal neurons in these regions, potentially contributing to the pathophysiology of absence seizures.
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Food Chem Toxicol
January 2025
Department of Occupational and Environmental Health, School of Public Health, Jinzhou Medical University, Jinzhou, Liaoning, PR China. Electronic address:
Flame retardant polybrominated diphenyl ethers (PBDEs) accumulate in human bodies through food and dust ingestion, and cause neurobehavioral deficits with obscure mechanism. We aimed to investigate NMDAR-CaMKⅡγ-mediated synapse-to-nuclear communication involved in BDE-209-induced cognitive impairment, and alleviation from exogenous melatonin. Decreased NMDAR subunits GluN2A and 2B, autophosphorylation of CaMKⅡα, and postsynaptic GluA1 trafficking were observed in the hippocampus of juvenile rats after maternal BDE-209 exposure.
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Sci Rep
January 2025
Laboratory of Biomedical Imaging and Data Analysis, Institute of Biomedical Systems and Biotechnology, Peter the Great St. Petersburg Polytechnic University, Khlopina St. 11, St. Petersburg, Russia, 194021.
One of the mechanisms of calcium signalling in neurons is store-operated calcium entry (SOCE), which is activated when the calcium concentration in the smooth endoplasmic reticulum (ER) decreases and its protein-calcium sensor STIM (stromal interacting molecule) relocate to the endoplasmic reticulum and plasma membrane junctions, forms clusters and induces calcium entry. In electrically non-excitable cells, STIM1 is coupled with the positive end of a tubulin microtubule through interaction with EB1 (end-binding) protein, which controls its oligomerization, SOCE and participates in ER movement. STIM2 homologue, which is specific for mature hippocampal dendritic spines, is known to interact with EB3 protein, however, not much is known about the role of this interaction in STIM2 clustering or ER trafficking in neurons.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Center for Neuroscience, University of California, Davis, CA 95618.
How newly formed memories are preserved while brain plasticity is ongoing has been a source of debate. One idea is that synapses which experienced recent plasticity become resistant to further plasticity, a type of metaplasticity often referred to as saturation. Here, we probe the local dendritic mechanisms that limit plasticity at recently potentiated synapses.
View Article and Find Full Text PDFBiomolecules
December 2024
Inst Neurophysiopathol, CNRS, INP, Aix-Marseille Univ, 13005 Marseille, France.
We previously reported that membrane-type 5-matrix metalloproteinase (MT5-MMP) deficiency not only reduces pathological hallmarks of Alzheimer's disease (AD) in 5xFAD (Tg) mice in vivo but also impairs interleukin-1 beta (IL-1β)-mediated neuroinflammation and Aβ production in primary Tg immature neural cell cultures after 11 days in vitro. We now investigate the effect of MT5-MMP on incipient pathogenic pathways that are activated in cortical primary cultures at 21-24 days in vitro (DIV), during which time neurons are organized into a functional mature network. Using wild-type (WT), MT5-MMP (MT5), 5xFAD (Tg), and 5xFADxMT5-MMP (TgMT5) mice, we generated primary neuronal cultures that were exposed to IL-1β and/or different proteolytic system inhibitors.
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