cctk convfac The factor between convergence levels. The base level is 0, and every level above that is coarsened by a factor of cctk convfac. cctk convlevel The convergence level of this grid hierarchy. The following variables are used for identifying convergence levels. The integer factor by which the time step size is reduced with respect to the base grid. The distance in direction dir is given by 1.0 * cctk levoff / cctk levoffdenom. and cctk levoffdenom Two arrays of cctk dim integers describing the distance by which the local grid is offset with respect to the base grid, measured in local grid spacings. APPLICATION THORNS The following variable is needed for grid refinement methods cctk levfac cctk levoff cctk timefac An array of cctk dim integer factors by which the local grid is refined in the corresponding direction with respect to the base grid. To enable us to ensure you receive communications that are relevant to you, please tell us which of the following areas you are interested in.C1.6.
(Kaneko et al., 2022)Īt Scientifica we take your privacy seriously and will only use your personal information to provide the products and services you have requested from us. 2 (in black), which produce depolarization in cells no. Four synaptic connections were identified from cell no. 6) in the mini-slice preparation under infrared differential interference contrast (IR-DIC) and corresponding epifluorescence (1 showing tdTomato-positive PV-INs). Shown is a representative image of two PV-INs (cells no. Learn More Multiple whole-cell recording from tdTomato-positive PV-INs as well as principal cells. These results demonstrate dynamic dysfunction in Dravet syndrome: combined abnormalities of PV-IN spike generation and propagation drives early disease severity, while ongoing dysfunction of synaptic transmission contributes to chronic pathology. Modeling confirms that PV-IN axonal propagation is more sensitive to decreased sodium conductance than spike generation.
However, PV-IN synaptic transmission is dysfunctional in young Scn1a+/− mice that did not survive and in Scn1a+/− mice ≥ P35. An approach assessing PV-IN function in the same mice at two time points shows impaired spike generation in all Scn1a+/− mice at postnatal days (P) 16–21, whether deceased prior or surviving to P35, with normalization by P35 in surviving mice. Nav1.1-expressing parvalbumin GABAergic interneurons (PV-INs) from young Scn1a+/− mice show impaired action potential generation. Dravet syndrome is a neurodevelopmental disorder characterized by epilepsy, intellectual disability, and sudden death due to pathogenic variants in SCN1A with loss of function of the sodium channel subunit Nav1.1.
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