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Evaluation of Water and Its Contaminants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
The autoradiographic distribution of STX binding sites associated with the voltage-sensitive Na+ channel was studied in the cerebellum of the neurological weaver (wv/wv), Purkinje cell degeneration (pcd/pcd), nervous (nr/nr), and reeler (rl/rl) mutant mice. The Purkinje cell layer contains the highest density of STX binding sites in normal mice. High densities were observed in the molecular layer. Intermediate and very low densities were present in the granular layer and the white matter, respectively. There was an important decrease in grain density in the molecular layer and Purkinje cell layer of the cerebellum, where a large majority of granular cells had disappeared. A small decrease was observed in the Purkinje cell layer where the Purkinje cells had almost all degenerated. Mutants where all neuronal cells were malpositioned, the compacted molecular layer contained an increased STX binding sites density. Conversely, the labeling of Purkinje cells areas was decreased. The hippocampal formation of mutants presents a homogeneous repartition of the Na+ channel protein, in contrast with the laminated distribution observed in normal mice. Our autoradiographic data suggest that a major proportion of STX-sensitive Na+ channels are localized in parallel fibers of granular cells and in axons of basket cells in a presynaptic position. In Purkinje cells, the dendritic arborization seems to be devoid of STX binding sites conversely to somata.
Continuum modeling for neuronal lamination during cerebral morphogenesis considering cell migration and tissue growth
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2021
Hironori Takeda, Yoshitaka Kameo, Taiji Adachi
To understand the essential mechanism of the inside-out neuronal lamination, the migration and accumulation of neurons is simulated using a one-dimensional model with a coordinate (Figure 1). Previous studies (D'Arcangelo and Curran 1998; Caffrey et al. 2014) proposed that the inside-out lamination may be achieved through the attractive effect of reelin, which enables the late-born neurons to migrate from the VZ to MZ through the accumulated early-born neurons (Figure 1, middle panel). The lack of expression of reelin in the reeler cerebrum disrupts the neuronal migration, thus resulting in inverted lamination (Figure 1, bottom panel).