Fig. 5
From: Hypothalamic neuronal circuits regulating hunger-induced taste modification
Vglut2 neurons are necessary for hunger-induced modulation of taste preference. a Bilateral injection of AAV-DIO-hM4Di-mCherry or AAV-DIO-hM3Dq-mCherry into the LHA of Vglut2-ires-Cre mice. b–c Representative images of hM4Di-mCherry (b) and hM3Dq-mCherry (c) expression in Vglut2LHA neurons. Fx, fornix. d Chemogenetic inhibition (CNO 1.0 mg/kg i.p.) of Vglut2 neurons in the LHA promotes food intake in Vglut2-hM4Di mice within 1 h n = 7, paired Student’s t test. e–f Brief access tests with sweet (e) and bitter (f) taste solutions in Vglut2LHA-hM4Di mice in the presence or absence of CNO (1.0 mg/kg i.p.). n = 6, F = 11.99, and P = 0.001 in e and n = 6, F = 5.37, and P = 0.023 in f, two-way ANOVA with Bonferroni post hoc test. g Chemogenetic activation (CNO 1.0 mg/kg i.p.) of Vglut2 neurons in the LHA led to a decrease in 1-h food intake in 23-h-fasted Vglut2LHA-hM3Dq mice. h–i Brief access test with sweet (h) and bitter (i) taste solutions in Vglut2LHA-hM3Dq mice under fed or 23-h-fasted conditions in the presence or absence of CNO (1.0 mg/kg i.p.). n = 6, F = 21.77, and P = 1.5 × 10–8 in h and n = 6, F = 19.51, and P = 1.1 × 10–7 in i, two-way ANOVA with Bonferroni post hoc test. All experiments were carried out with 10- to 16-week-old male mice. Data are given as means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, as compared with the saline group (d–g) and with the fasted (saline) group (h–i)
