Evaluation of dendrite morphology in Wistar and genetic absence epileptic rats.

Brain Struct Funct

Department of Anatomy, School of Medicine, Marmara University, Istanbul, Turkey.

Published: December 2024

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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http://dx.doi.org/10.1007/s00429-024-02868-3DOI Listing

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