Fig. 7: AAV drives long-term GPR173 expression and does not induce abnormal firing properties in transfected excitatory neurons.
From: Upregulation of CCK3R leading to the suppression of chronic seizures
A Examples of action potential (AP) traces evoked by current injection in cortical excitatory neurons from the mice of saline, CaMKII-Sham-mCherry, CaMKII-GPR173-mCherry groups at the age of 6 months. B Line chart showing the frequency of APs in excitatory neurons from the above three groups of mice (two-way ANOVA with Tukey’s post hoc test, N.S.). C Histogram showing the amplitude of APs in response to 200 pA current injection in excitatory neurons from the three groups of mice (two-way ANOVA with Tukey’s post hoc test, N.S.). D Histogram showing the resting membrane potential in excitatory neurons from the three groups of mice (two-way ANOVA with Tukey’s post hoc test, N.S.). E Histogram showing half-width of the APs (two-way ANOVA with Tukey’s post hoc test, N.S.). F Histogram showing latency of the APs (two-way ANOVA with Tukey’s post hoc test, N.S.). In whole-cell patch-clamp recordings, n = 17–20 neurons per group. G Body weight changes of mice before and after tail vein injection (saline group, N = 9; CaMKII-Sham-mCherry group, N = 9; CaMKII-GPR173-mCherry group, N = 10; two-tailed two-sample t-test, *P < 0.05; N.S.). H The survival rate of mice from the start of tail vein injection until the perfusion period. Deaths due to Morris water maze test were not counted (Saline group, N = 9; CaMKII-Sham-mCherry group, N = 10; CaMKII-GPR173-mCherry group, N = 8). Data are shown as mean ± standard error of the mean. AAV adeno-associated virus, N.S. not significant.
