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Results: 4

1.
Fig. 2.

Fig. 2. From: Alteration of BACE1-dependent NRG1/ErbB4 signaling and schizophrenia-like phenotypes in BACE1-null mice.

Clozapine attenuates PPI deficits and hyperactivity in BACE−/−mice. Effect of clozapine (2 mg/kg, i.p.) on hyperactivity (A), PPI (B), and working-memory deficits (C) in BACE1−/− mice. PPI shows an overall percentage of inhibition (±SEM) observed in four types of trials with two different levels of startle and prepulse stimuli (Fig. S3). Abbreviations and signs are as in Fig. 1 (n = 8–12 per genotype per treatment).

A. V. Savonenko, et al. Proc Natl Acad Sci U S A. 2008 April 8;105(14):5585-5590.
2.
Fig. 4.

Fig. 4. From: Alteration of BACE1-dependent NRG1/ErbB4 signaling and schizophrenia-like phenotypes in BACE1-null mice.

Fine structure of CA1 dendrites in the hippocampus of BACE1−/− mice. (A and B) Representative images of dendrites from CA1 pyramidal neurons of WT (A) and BACE1−/− mice (B). (C) Spine density (per millimole) for WT and BACE1−/− neurons (n = 241 and 182, respectively). (D) Total spine number per dendrite (n = 909 and 658 dendrites for WT and BACE1−/−, respectively). (E) Proportions of mushroom-shaped spines (from a total pool of 10,637 and 4,648 spines for WT and BACE1−/−, respectively) were calculated for each neuron and are shown as function of neurons with different spine load. Asterisks indicate significant differences between WT and BACE1−/− measures (P < 0.05) as a result of ANOVA (C and D) or post hoc tests applied to a significant effect of ANOVA (E).

A. V. Savonenko, et al. Proc Natl Acad Sci U S A. 2008 April 8;105(14):5585-5590.
3.
Fig. 3.

Fig. 3. From: Alteration of BACE1-dependent NRG1/ErbB4 signaling and schizophrenia-like phenotypes in BACE1-null mice.

BACE1-related changes in NRG1 processing and ErbB4–PSD95 association. (A) Western blots of cortex homogenates from BACE1−/− and WT littermates stained with antibodies for C-terminal fragment of NRG1, MBP, and SOD1. (B) Bar graphs of relative NRG1-CTF, MBP, and SOD1 protein levels (mean ± SEM) based on results in A. (C) Western blot of cortex homogenates stained for PSD95 before (Top) and after (Bottom) immunoprecipitation with ErbB4 antibody. Middle shows Western blot for ErbB4 in samples after immunoprecipitation with ErbB4 antibody. Two bands represent full-length mature ErbB4 receptor (≈180 kDa) and its less-glycosylated intermediate (≈160 kDa) (39). (D) Bar graphs of PSD95 protein levels relative to GAPDH (Top) or ErbB4 (Bottom) and protein levels of ErbB4 (Middle). Open and closed bars represent measures for WT and BACE−/− mice, respectively. WB, Western blotting; IP, immunoprecipitation.

A. V. Savonenko, et al. Proc Natl Acad Sci U S A. 2008 April 8;105(14):5585-5590.
4.
Fig. 1.

Fig. 1. From: Alteration of BACE1-dependent NRG1/ErbB4 signaling and schizophrenia-like phenotypes in BACE1-null mice.

Schizophrenia-like phenotypes of BACE1−/− mice. (A) Deficit in prepulse inhibition of acoustic startle reaction. (B) Hypersensitivity to the effects of (+)-MK-801 (0.3 mg/kg, i.p.) on locomotor activity. (C) Dynamics of locomotor activity after PBS or MK-801 injection. (D) Deficits in social recognition. Changes in time of social investigation are shown for habituation and dishabituation phases of the task (see SI Materials and Methods). C57B6 and SW denote a strain background of juvenile stimulus mice. Test mice were C57B6 background. (E) Working-memory deficits tested in the radial water maze (2). Note that the BACE1−/− mice were impaired in working-memory errors (reentries into previously visited arms) but were not different from other genotypes in long-term memory errors. (F) Deficit in the inhibitory avoidance. The latencies to stepdown from an elevated platform are shown for training and testing trial separated by 48-h delay. BACE1−/− mice had preserved sensitivity to a foot shock (Fig. S2). Data are expressed as means ± SEM. Triangles and asterisks indicate significant differences of BACE1−/− mice from WT or BACE1+/− littermates, respectively, as a result of Newman–Keuls post hoc test applied to significant effect of genotype or interactions (ANOVA, n = 8–12 mice per genotype).

A. V. Savonenko, et al. Proc Natl Acad Sci U S A. 2008 April 8;105(14):5585-5590.

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