Figure 3.
Neuronal dysfunction in TDPΔCR mice without TDP-43 proteinopathy or neurodegeneration. (A) Representative images of immunohistochemical staining of TDP-43 in the hippocampus, cortex, and spinal cord neuronal cells of WT and TDPΔCR+/− mice. (B) Representative images and quantification of immunohistochemical staining of NeuN in the hippocampus, cortex, and spinal cord of WT and TDPΔCR+/− mice (n = 6 mice per group). (C) Representative Golgi staining images and quantification of CA1 pyramidal neurons from WT mice (n = 14 neurons from 3 mice) and TDPΔCR+/− mice (n = 15 neurons from 3 mice). (D) Representative photomicrographs and Sholl analysis of CA1 pyramidal neurons from WT (n = 14 neurons from 3 mice) and TDPΔCR+/− mice (n = 15 neurons from 3 mice). (E) Representative images and quantification of apical dendritic spines from CA1 pyramidal neurons of WT and TDPΔCR+/− mice (n = 300–327 spines from 3 mice per group). (F) Slope of fEPSP after high-frequency stimulation of fEPSP in CA3–CA1 regions of WT (n = 22 slices from 7 mice) and TDPΔCR+/− mice (n = 16 slices from 7 mice), normalized by baseline. (G) I/O curve of fEPSP in CA3–CA1 regions of WT (n = 22 slices from 7 mice) and TDPΔCR+/− mice (n = 16 slices from 7 mice), normalized by fEPSP amplitude induced by minimum stimulation intensity. (H) Paired-pulse facilitation, elicited by application of two successive stimulation pulses to CA3 (interstimulus intervals between 50 and 250 ms), was measured as the amplitude ratio of the second fEPSP divided by the first fEPSP in a pair. Data are mean ± SEM; two-tailed Student’s t test (B, C, and E) or two-way ANOVA followed by Bonferroni multiple comparisons test (D, G, and H). *, P < 0.05; ***, P < 0.001; and ****, P < 0.0001.

Neuronal dysfunction in TDPΔCR mice without TDP-43 proteinopathy or neurodegeneration. (A) Representative images of immunohistochemical staining of TDP-43 in the hippocampus, cortex, and spinal cord neuronal cells of WT and TDPΔCR+/− mice. (B) Representative images and quantification of immunohistochemical staining of NeuN in the hippocampus, cortex, and spinal cord of WT and TDPΔCR+/− mice (n = 6 mice per group). (C) Representative Golgi staining images and quantification of CA1 pyramidal neurons from WT mice (n = 14 neurons from 3 mice) and TDPΔCR+/− mice (n = 15 neurons from 3 mice). (D) Representative photomicrographs and Sholl analysis of CA1 pyramidal neurons from WT (n = 14 neurons from 3 mice) and TDPΔCR+/− mice (n = 15 neurons from 3 mice). (E) Representative images and quantification of apical dendritic spines from CA1 pyramidal neurons of WT and TDPΔCR+/− mice (n = 300–327 spines from 3 mice per group). (F) Slope of fEPSP after high-frequency stimulation of fEPSP in CA3–CA1 regions of WT (n = 22 slices from 7 mice) and TDPΔCR+/− mice (n = 16 slices from 7 mice), normalized by baseline. (G) I/O curve of fEPSP in CA3–CA1 regions of WT (n = 22 slices from 7 mice) and TDPΔCR+/− mice (n = 16 slices from 7 mice), normalized by fEPSP amplitude induced by minimum stimulation intensity. (H) Paired-pulse facilitation, elicited by application of two successive stimulation pulses to CA3 (interstimulus intervals between 50 and 250 ms), was measured as the amplitude ratio of the second fEPSP divided by the first fEPSP in a pair. Data are mean ± SEM; two-tailed Student’s t test (B, C, and E) or two-way ANOVA followed by Bonferroni multiple comparisons test (D, G, and H). *, P < 0.05; ***, P < 0.001; and ****, P < 0.0001.

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