Fig. 3.

Intranasal administration of oxytocin in an AD model increases expression of mTOR. The expression of several mediators in the oxytocin-OXTR pathway was measured in hippocampal tissue isolated from oxytocin- or vehicle-treated AD and wild type mice after 42 days of treatment. Expression was normalized using GAPDH and HPRT1 and converted to fold change values (as compared to WT control animals). Expression of mTOR was upregulated in the AD group that received oxytocin (n = 8) compared to the AD control group (a) (n = 8) (two-way ANOVA with Tukey post-hoc analysis). Expression of cFOS and PRKCZ was not significantly different in any condition (b, c). Bars represent mean±SEM. mTOR, mammalian target of rapamycin; PKMζ, protein kinase M ζ; AD, Alzheimer’s disease; OXTR, oxytocin receptor; GAPDH, glyceraldehyde-3-phosphate dehydrogenase. **p < 0.005, *p < 0.05.