barnes maze behavioral circular apparatus  (San Diego Instruments)

Journal: NeuroSci

Article Title: Effect of High-Salt Diet on Memory and Behavior in Mice Expressing Human Apolipoprotein Epsilon-4 (APOE4) Allele

doi: 10.3390/neurosci7020043

Figure Lengend Snippet: Memory and learning: the male and female APOE3 and APOE4 mice were trained, and their memory and learning abilities were determined by the Barnes maze test. The bars represent latency to target hole (sec) data as the mean ± SE on normal-salt (0.4%), low-salt (0.1% NaCl) ( A ) and high-salt (4% NaCl) ( B ) diets, n = 7 in the low-salt treatment groups and n = 9 in the high-salt treatment groups. No sex differences were observed. Significance was calculated by Two-way ANOVA, followed by Bonferroni multiple comparison tests (* p < 0.05).

Article Snippet: The Barnes maze behavioral circular apparatus (San Diego Instruments (SDI), San Diego, CA, USA) was constructed of white ABS plastic and contained 20 circular holes (2-inch diameter), evenly spaced along the perimeter of the maze.

Techniques: Comparison

Journal: NeuroSci

Article Title: Effect of High-Salt Diet on Memory and Behavior in Mice Expressing Human Apolipoprotein Epsilon-4 (APOE4) Allele

doi: 10.3390/neurosci7020043

Figure Lengend Snippet: Memory in APOE3 and APOE4: 72 h after the 4th training day, memory to reach the target hole was measured by the Barnes maze test. Primary latency ( A , B ), primary errors ( C , D ), total nose pokes ( E , F ), and distance traveled ( G , H ) were measured. Each bar represents data as the mean ± SE, and n = 7 in the low-salt treatment groups and n = 9 in the high-salt treatment groups. No sex differences were observed. Significance was calculated by Two-way ANOVA, followed by Bonferroni multiple comparison tests. (* p < 0.05).

Article Snippet: The Barnes maze behavioral circular apparatus (San Diego Instruments (SDI), San Diego, CA, USA) was constructed of white ABS plastic and contained 20 circular holes (2-inch diameter), evenly spaced along the perimeter of the maze.

Techniques: Comparison

Journal: bioRxiv

Article Title: Age-specific Aβ-Tau interactions underlie spatial memory deficits in an APP/PS1 amyloidosis model

doi: 10.64898/2025.12.06.689974

Figure Lengend Snippet: Primary latency, defined as the time required for a mouse to reach the target hole for the first time, was measured in wild-type (WT, open squares) and APP/PS1 transgenic (TG, filled squares) mice during three consecutive training days (five trials per day) in the Barnes maze. At 6 and 12 months of age, no significant differences in primary latency were observed between WT and TG mice, indicating preserved learning performance. At 18 months, TG mice exhibited significantly longer latencies compared to age-matched WT controls on training days 1 and 2 ( P <0.01; LSD post hoc test). The insets show mean primary latency (±SEM) for each training day across ages, with 18-month-old TG mice performing worse than 6-month-old animals. Repeated-measures ANOVA confirmed significant main effects of genotype [F(1,51)=4.7; P <0.05] and significant trial day x age interaction effects on the primary latency of TG and WT animals [F(2,51)=7.5; P <0.01]. Data are expressed as mean ± SEM (n = 9-11 per group).

Article Snippet: The Barnes maze apparatus (Panlab S.L.U., Barcelona, Spain) was a circular platform with 20 equidistant holes around its perimeter, elevated 1.5 m above the floor and brightly illuminated by four 120W halogen lamps, to create an aversive environment.

Techniques: Transgenic Assay

Journal: bioRxiv

Article Title: Age-specific Aβ-Tau interactions underlie spatial memory deficits in an APP/PS1 amyloidosis model

doi: 10.64898/2025.12.06.689974

Figure Lengend Snippet: The spatial distribution of nose-pokes across all holes of the Barnes maze was analyzed in wild-type (WT, open circles) and APP/PS1 transgenic (TG, filled circles) mice during the probe trials, which were conducted 24 hours (Day 4) and 8 days (Day 11) after training. The dashed horizontal line represents the level of nose-poking expected by chance (random performance). Insets show the total number of nose-pokes performed during each session. (A) At 6 months of age, WT and TG mice showed comparable search patterns and similar total nose-poke counts. (B) At 12 months, TG mice made significantly fewer nose-pokes in the target hole compared to WT animals on Day 11 ( P <0.01–0.001), indicating impaired memory for the target location. (C) At 18 months, TG mice exhibited impaired spatial memory, as shown by reduced preference for the target hole compared to WT mice on Day 4 ( P <0.001). WT animals also showed reduced target-directed responding between Days 4 and 11 ( P <0.01). Repeated measures ANOVA confirmed significant main effects of genotype [F(1,102)=8.4; P <0.01] and age [F(2,102)=6.6; P <0.01] on the distribution of nose-pokes, along with significant hole x genotype [F(19,1938)=7.2; P <0.001], hole x age [F(38,1938)=3.1; P <0.001] and hole x trial day interaction effects [F(19,1938)=3.3; P <0.001]. Data are expressed as mean ± SEM of n = 9-11 mice per group.

Article Snippet: The Barnes maze apparatus (Panlab S.L.U., Barcelona, Spain) was a circular platform with 20 equidistant holes around its perimeter, elevated 1.5 m above the floor and brightly illuminated by four 120W halogen lamps, to create an aversive environment.

Techniques: Transgenic Assay

Journal: bioRxiv

Article Title: Age-specific Aβ-Tau interactions underlie spatial memory deficits in an APP/PS1 amyloidosis model

doi: 10.64898/2025.12.06.689974

Figure Lengend Snippet: Pearson correlation analyses between Barnes maze performance and neuropathological measures in 6-, 12-, and 18-month-old APP/PS1 transgenic mice. Significant negative correlations were observed between Aβ plaque load and target block time in all cortical regions and the hippocampus (r = −0.43 to −0.63, P <0.05–0.001), indicating that higher amyloid burden was associated with poorer spatial memory performance. (B) [ 18 F]Flortaucipir binding also correlated negatively with target block time in all regions analyzed (r = −0.50 to −0.57, P <0.01), linking increased tau accumulation with cognitive impairment. (C) [ 3 H]UCB-J binding, a marker of synaptic density, showed weaker correlations, reaching significance only in the frontal (r = −0.45, P <0.05) and parietal/temporal cortices (r = −0.38, P<0.05). Scatter plots on the right illustrate representative correlations between target block time and the total levels of each pathological marker in the brain.

Article Snippet: The Barnes maze apparatus (Panlab S.L.U., Barcelona, Spain) was a circular platform with 20 equidistant holes around its perimeter, elevated 1.5 m above the floor and brightly illuminated by four 120W halogen lamps, to create an aversive environment.

Techniques: Transgenic Assay, Blocking Assay, Binding Assay, Marker

Journal: JCI Insight

Article Title: Mapping SCA1 regional vulnerabilities reveals neural and skeletal muscle contributions to disease

doi: 10.1172/jci.insight.176057

Figure Lengend Snippet: ( A ) Organization of the mouse WT-Atxn1 (blue) and human ATXN1 (black) genes, with the only 2 exons encoding the ATXN1 protein indicated by boxes larger and darker than the noncoding exons. The size (kb) and location of the mouse genomic sequences (blue) replaced by the human genomic sequences (black) in the f-ATXN1 146Q allele are indicated. ( B ) The portion of the Atxn1 gene encompassing the 2 coding exons was replaced with an FRT-recombination recipient cassette in mouse ES cells; then, that cassette was replaced with the portion of the human ATXN1 genomic sequences syntenic to the deleted mouse sequence using FLP recombinase. ( C ) The inserted human sequences in the resulting ATXN1 146Q allele are flanked by LOX recombination sites, as shown. Mating mice with this allele to lines expressing CRE recombinase removes the human ATXN1 insertion, as shown. ( D ) Barnes maze performance at 24 weeks of age, using unpaired 2-tailed t test. ( E ) Mouse survival plotted as Kaplan-Meier curves with median lifespan labeled for each genotype. Log-rank (Mantel Cox) **** P < 0.0001 and Gehan-Breslow-Wilcoxon #### P < 0.0001. ( F ) Body weight measurements between 6 and 36 weeks of age, repeated-measures 2-way ANOVA with Geisser-Greenhouse correction and Šídák’s post hoc test. ( G ) Representative photographs of 42-week-old WT-Atxn1 2Q/2Q and f-ATXN1 146Q/2Q showing kyphosis. * P < 0.05, ** P < 0.01, and **** P < 0.0001.

Article Snippet: A Barnes maze apparatus (San Diego Instruments) was used to assess spatial learning and memory ( ).

Techniques: Genomic Sequencing, Sequencing, Expressing, Labeling

Journal: JCI Insight

Article Title: Mapping SCA1 regional vulnerabilities reveals neural and skeletal muscle contributions to disease

doi: 10.1172/jci.insight.176057

Figure Lengend Snippet: ( A ) Open-field performance at 12 weeks of age, using 1-way ANOVA Tukey’s post hoc test. ( B ) Barnes maze performance at 24 weeks of age, using 1-way ANOVA Tukey’s post hoc test. ( C ) Mouse survival plotted as Kaplan-Meier curves with median lifespan labeled for each genotype. Log-rank (Mantel Cox) **** P < 0.0001 and Gehan-Breslow-Wilcoxon #### P < 0.0001. ( D ) Body weight measurements between 7 and 48 weeks of age. Significant weight difference shown is between f-ATXN1 146Q/2Q and f-ATXN1 146Q/2Q ;Nestin-Cre at 38 weeks. Repeated-measures 2-way ANOVA Geisser-Greenhouse correction and Tukey’s post hoc test. ( E ) Hind limb clasping at 36 weeks. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: A Barnes maze apparatus (San Diego Instruments) was used to assess spatial learning and memory ( ).

Techniques: Labeling