Journal: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
Article Title: Hypophagia induced by hindbrain serotonin is mediated through central GLP-1 signaling and involves 5-HT2C and 5-HT3 receptor activation.
doi: 10.1038/s41386-019-0384-x
Figure Lengend Snippet: Fig. 4 Activation of hindbrain 5-HT3R suppresses chow intake and is dependent on central GLP-1 signaling. The 5-HT3R agonist, SR57227 (SR5) was delivered (4th ICV) using the following doses: 0 (aCSF), 5, 10, or 20 µg a–c (n = 11). Only the highest dose (20 µg) of SR5 suppresses chow intake, this suppression was significant at all timepoints. a A 20 µg treatment with SR5(4th ICV) prevents BW gain seen in the control group b and increases kaolin intake c (n = 21). The effect of central blockade of GLP-1Rs was tested in a separate cohort (n = 19). Treatment with Ex9 reverses the anorectic effect of SR5 at 6 and 24 h, but not at 1 and 3 h d (n = 19). SR5 and Ex9 alone or in combination have no effect on 24 h body weight e or kaolin intake f. A repeated measures one-way ANOVA and Dunnet post hoc (*p < 0.05, **p < 0.01) was used in 3a, whereas a paired t test was used for b–c. Data in d–f were analyzed using a two-way ANOVA, different letters are significantly different from each other (p < 0.05) according to Newman–Keuls post hoc analyses
Article Snippet: Drugs and delivery sites The competitive GLP-1R antagonist, exendin-(9–39) (Ex9; Bachem, 4017799), serotonin chloride (5-HT; Tocris, 3547), selective 5- HT2CR agonist, lorcaserin (Lor; KeyOrganics, KS1439), and selective 5-HT3R agonist, SR57227 (SR5; Tocris, 1205), were all dissolved in artificial cerebrospinal fluid (aCSF; Harvard Apparatus, 59–7316).
Techniques: Activation Assay, Control