Synaptic potentiation induced by forskolin at mossy fiber synapse.

<p>(A) Pooled data showing potentiation of mossy fiber synaptic transmission by bath-applied forskolin (10 µM). There was no significant difference in the magnitude of potentiation between wild-type and mutant mice (<i>p</i> = 0.6905, n = 5 each). The effect of serotonin examined in the same mice was shown in (B) and was larger in mutant mice (<i>p</i> = 0.0159). (B) Significant correlation between serotonin- and forskolin-induced synaptic potentiation in mutant mice (r² = 0.8177, <i>p</i> = 0.00351), but not in wild-type mice (r² = 0.5067, <i>p</i> = 0.1775).</p

Reduced hippocampal expression of dopamine D1 receptor in sandy mice.

<p>(A) Expression levels of mRNAs for serotonin 5-HT₄ receptor relative to those of GAPDH in the hippocampus (n = 10 each). (B) Relative expression levels of mRNAs for dopamine D₁ receptor in the hippocampus were reduced in mutant mice as compared with wild-type mice (+/+: 6.04±0.17; −/−: 5.16±0.2, n = 10 each; <i>p</i> = 0.0068).</p

Basic properties of synaptic transmission at mossy fiber synapse.

<p>(A) Input-output relationship at the mossy fiber-CA3 synapse. The amplitude of the presynaptic fiber volley (left) and fEPSP (right) was plotted against the stimulus intensity (n = 15 slices each). (B) Frequency facilitation induced by repetitive stimulation was reduced in mutant mice at the stimulus frequency of 0.2 Hz (+/+: 54.0±2.8% increase, n = 8; −/−: 42.9±3.3% increase, n = 11; <i>p</i> = 0.039), but not at 1 Hz (+/+: n = 7; −/−: n = 10). (C) No significant difference in facilitation of fEPSP induced by paired stimulation (+/+: n = 8; −/−: n = 9).</p

Passive and active somatic membrane properties of dentate granule cells.

<p>(A) Reduced input resistance in mutant mice (+/+: 494.8±48.4 MΩ, n = 12 cells; −/−: 373.6±33.4 MΩ, n = 14 cells; <i>p</i> = 0.0477).v (B) Shorter membrane time constant in mutant mice (+/+: 33.2±2.2 ms; −/−: 24.9±1.4 ms; <i>p</i> = 0.0109). (C–F) There was no significant difference in resting membrane potentials (C), the current intensity to evoke a single spike (D), the maximal number of spikes during sustained depolarization (E), or spike amplitude (F).</p

Impact of the <i>NRGN</i> genotype on GM volume of left anterior cingulate gyrus in schizophrenia.

<p>(<b>A</b>) Anatomical localizations are displayed on coronal, sagittal, and axial sections of a normal MRI spatially normalized into the Montreal Neurological Institute template (uncorrected <i>p</i><0.001, cluster size>100). A significant cluster of the genotype effect was in the left anterior cingulate gyrus in the patients with schizophrenia, after controlling for differences in the duration of illness among genotypes. The region is shown as cross-hairline. The color bars show <i>t</i> values corresponding to the color in the figure. (<b>B</b>) Each column shows relative gray matter volumes extracted from the left anterior cingulate gyrus (Talairach coordinates; −12, 42, −9). We extracted a sphere with a 10 mm volume-of-interest (VOI) radius from the significant region to compare the effects of the genotype in both the patients with schizophrenia and healthy subjects. Error bars represent the standard error.</p

Effects of <i>NRGN</i> genotype and genotype-diagnosis interaction on GM and WM volumes in total subjects.

<p>GM: gray matter, WM: white matter, R: right, L: left, BA: Brodmann area, CS: Cluster size, FWE: family-wise error.</p

Effects of <i>NRGN</i> genotype on GM volumes in patients with schizophrenia and in healthy controls.

<p>GM: gray matter, R: right, L: left, BA: Brodmann area, CS: Cluster size, FWE: family-wise error, SZ: patients with schizophrenia, HC: healthy controls. Significant results [<i>p</i><0.05 (<i>FWE</i> corrected)] are shown as bold face and underline.</p

Effects of the risk-T-allele on decreased GM regions and diagnosis-<i>NRGN</i> genotype interaction on GM regions.

<p>Effects of the risk T allele on decreased GM regions (TTNRGN genotype interaction on GM regions was shown by hot colormap (red areas). There was no significant effect of the risk T allele on increased GM regions (CCt values corresponding to the color in the figure.</p

Genotypic and allelic distributions for SNPs in the <i>p250GAP</i> between patients with schizophrenia and controls.

<p>SCZ: patients with schizophrenia, CON: controls, M: major allele, m: minor allele, MAF: minor allele frequency, OR: odds ratio, 95%CI: 95% confidence interval.</p>a<p>db SNP build 129.</p><p>All of the alleles are represented according to the minus strand DNA sequence. Numbers of genotypes were represented as genotype counts. <i>P</i> values<0.05 are in boldface and underlined.</p

The association between the risk-associated <i>p250GAP</i> genotype and SPQ total score and the three factors.

<p>The gray bars represent individuals who are G-carriers (G/G and G/A genotypes) of rs2298599. The white bars represent individuals with the A/A genotype of the SNP. Error bars represent standard errors of the mean. * <i>p</i><0.05.</p