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Results: 5

1.
Figure 1

Figure 1. Deletion of APLP2 does not affect spine density in primary culture. From: Deletion of the amyloid precursor-like protein 2 (APLP2) does not affect hippocampal neuron morphology or function.

A) Representative images of cultured primary hippocampal neurons that were transfected with eGFP at DIV 15–18, fixed and imaged one day post transfection. Insets show the segments in the secondary dendrites that were quantified for spine numbers after magnification. B) Quantification of spine numbers from cultured neurons shown in (A). There were no differences in spine density between the two genotypes (wt: 41 neurons from n = 11 mice, APLP2−/−: 56 neurons from n = 13 mice.

Brea Midthune, et al. Mol Cell Neurosci. ;49(4):448-455.
2.
Figure 2

Figure 2. Aged APLP2−/− mice exhibit normal spine density, volume and morphometry. From: Deletion of the amyloid precursor-like protein 2 (APLP2) does not affect hippocampal neuron morphology or function.

A) Representative 3-dimensional reconstructions of CA1 pyramidal dendritic segments from 10–12 month old wt and APLP2−/− mice. B) Automated analysis of spine density displayed no changes in total spine density or in percentage of spine type per dendritic segment (5 wt and 7 APLP2−/− mice, at least 5 neurons per mouse and at least 3 dendritic segments per neuron). C) Further morphometric analysis of spine volume revealed comparable mean spine volumes amongst spine types.

Brea Midthune, et al. Mol Cell Neurosci. ;49(4):448-455.
3.
Figure 5

Figure 5. APLP2−/− mice show normal LTP in young and aged mice. From: Deletion of the amyloid precursor-like protein 2 (APLP2) does not affect hippocampal neuron morphology or function.

After a 20-minute baseline, LTP was induced by four 1-s tetanic stimuli delivered 5 minutes apart, each at 100 Hz. The percent increase in response after the tetanus was given was compared between the APLP2−/− mice and littermate animals at 1–2 months of age (A; 14 wt, 15 APLP2−/− slices from 10–12 animals/genotype) and at 10–12 months of age (B; 11 wt, 12 APLP2−/− slices from 6 – 7 animals/genotype). No significant difference was found across genotype or age group. Sample tracings to the right of each figure. Values represent mean ± SEM.

Brea Midthune, et al. Mol Cell Neurosci. ;49(4):448-455.
4.
Figure 3

Figure 3. Morphological alterations and dendritic length are not affected by the absence of APLP2 in aged animals in vivo. From: Deletion of the amyloid precursor-like protein 2 (APLP2) does not affect hippocampal neuron morphology or function.

Representative examples of 3D reconstructions from pyramidal layer CA1 neurons in 10-month-old wt control (A) and APLP2−/− (B) mice. Reconstructed cells were obtained using NeuroExplorer (MBF) and rotated about the principal axis to depict apical and basal dendritic orientation. Total dendritic length (C), Sholl analyses (dendritic length per radial distance from soma (D)) and intersections per radial distance from the soma were compared from apical dendrites of CA1 pyramidal cells of APLP2−/− mice and their wt littermates at 10–12 months of age revealing no significant difference between genotype. Cells were traced using Neurolucida and quantified using NeuroExplorer software (n=5 wt and 7 APLP2−/− mice). Values represent mean ± SEM.

Brea Midthune, et al. Mol Cell Neurosci. ;49(4):448-455.
5.
Figure 4

Figure 4. Deletion of APLP2 does not alter basal synaptic transmission in young or aged mice. From: Deletion of the amyloid precursor-like protein 2 (APLP2) does not affect hippocampal neuron morphology or function.

A) Scatter plots of the fEPSP amplitude versus fiber volley for 1–2 month old and 10–12 month old APLP2−/− and wt mice, fit by linear regression, demonstrated no significant difference in the input/output ratio between genotypes of young (A) or aged (B) animals (A; 14 wt, 15 APLP2−/− slices from 10 and 12 animals, respectively, B; n=11 wt, n=12 APLP2−/− slices from 6 and 7 animals respectively. Presynaptic release probability was examined by eliciting a second pulse 50 ms after the first pulse. No significant differences were found between genotypes at 1–2 months of age (C; 14 wt, 15 APLP2−/− slices from 10 and 12 animals, respectively) or 10–12 months of age (D; 11 wt, 12 APLP2−/− slices from 6 and 7 animals, respectively). Sample tracings located above the graph. Values represent mean ± SEM.

Brea Midthune, et al. Mol Cell Neurosci. ;49(4):448-455.

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