Article Figures & Data
Figures
- Fig. 1.
[3H]MK-801 binding in forebrain synaptic membranes of GluRε1 mutant mice. Triton-treated forebrain synaptic membranes were incubated with 5 nm[3H]MK-801 at 30°C for 16 hr, in the presence or absence of 10 μm glutamate (Glu), Glu plus 10 μm glycine (Gly), or Glu plus Gly plus 1 mm spermidine (SPD). Each column represents the mean ± SEM (n = 4). *p < 0.05; **p < 0.01 versus wild (+/+).
- Fig. 2.
NMDA-stimulated45Ca2+ uptake into forebrain synaptosomes of GluRε1 mutant mice. The forebrain synaptosomes were preincubated at 37°C for 10 min, in the presence or absence of 100 μm MK-801. The assay was initiated by adding prewarmed buffer containing 1 μCi/ml 45CaCl2 for 5 min, in the presence of 100 μm NMDA, NMDA plus 10 μm Gly, or NMDA plus Gly plus 1 mm SPD. Each column represents the mean ± SEM (n = 6). **p < 0.01, ***p < 0.001 versus wild (−MK-801).
- Fig. 3.
Monoamine metabolism in various brain regions of GluRε1 mutant mice. The tissue contents of monoamine and its metabolite in various brain regions were measured by HPLC with an electrochemical detector. a, MHPG/NE; b,DOPAC/DA; c, HVA/DA; d, 5-HIAA/5-HT. Each column represents the mean ± SEM (n = 7–8). *p < 0.05; **p < 0.01 versus wild (+/+).
- Fig. 4.
NMDA-stimulated [3H]dopamine, [14C]serotonin, and [3H]GABA release in GluRε1 mutant mice. The cortical and striatal slices were incubated with 1 μm[3H]DA, 1 μm[14C]5-HT, and 10 μm pargyline at 37°C for 30 min. For [3H]GABA release, the striatal slices were incubated with 1 μm[3H]GABA and 100 μm amino-oxyacetic acid. After washes, the cortical and striatal slices were superfused with Krebs'–Ringer's solution buffer at 37°C and exposed to 25 mm KCl at t = 70 min and then to 100 μm NMDA at t = 90 min for 2 min. For [3H]DA release in the presence of (+)bicuculline (Bicu), the [3H]DA-labeled striatal slices were superfused with Krebs'–Ringer's solution buffer containing 10 μm (+)bicuculline until the end of the experiment. Each column represents the mean ± SEM (n = 7–8). *p < 0.05; ***p < 0.001 versus corresponding wild (+/+). #p < 0.05 versus NMDA-stimulated [3H]DA release in wild (+/+).
- Fig. 5.
Locomotor activity in a novel environment in GluRε1 mutant mice. Locomotor activity and the number of rearing events in a novel environment were measured every 5 min for 120 min. Each column represents the mean ± SEM (n = 12). An ANOVA with repeated measures revealed a significant difference in locomotion (F(1,22) = 3.470;p = 0.0002) and rearing curves (F(1,22) = 2.028; p= 0.0265). **p < 0.01 versus wild (+/+).
- Fig. 6.
Effects of haloperidol and risperidone on the increased locomotor activity in GluRε1 mutant mice. Haloperidol (0.003 or 0.01 mg/kg, p.o.) or risperidone (0.01 or 0.03 mg/kg, p.o.) was administered 60 min before the measurement of locomotor activity in a novel environment. Each column represents the mean ± SEM (n = 8–10). ANOVA analysis:F(5,43) = 18.806, p< 0.0001 (locomotion-haloperidol);F(5,43) = 8.598, p< 0.0001 (rearing-haloperidol);F(5,51) = 15.205, p< 0.0001 (locomotion-risperidone);F(5,51) = 8.111, p< 0.0001 (rearing-risperidone). *p < 0.05 versus corresponding vehicle-treated wild (+/+). #p < 0.05; ##p < 0.01; ###p < 0.001 versus corresponding vehicle-treated GluRε1 (−/−).
- Fig. 7.
Latent learning in the water-finding task in GluRε1 mutant mice. The starting, entering, and finding latencies were measured in the test trial 24 hr after the training trial of the water-finding task. The starting, entering, and finding latencies in trained wild-type mice (+/+) were 2.1 ± 0.3, 9.0 ± 0.8, and 67.5 ± 17.9 sec, respectively. Each column represents the mean ± SEM (n = 12). *p< 0.05; **p < 0.01 versus corresponding nontrained group. #p < 0.05; ##p < 0.01 versus trained wild (+/+).
