1. Volume 123, Issue 4, Pages 1120-1128 (October 2002)
The role of the gastric afferent vagal nerve in ghrelin-induced feeding and growth hormone secretion in rats 
Yukari Date, Noboru Murakami, Koji Toshinai, Shigeru Matsukura, Akira Niijima, Hisayuki Matsuo, Kenji Kangawa, Masamitsu Nakazato 
Gastroenterology 
Volume 123, Issue 4, Pages (October 2002)
DOI: /gast
Copyright © 2002 American Gastroenterological Association Terms and Conditions

2. Fig. 1
Effect of vagotomy or capsaicin treatment on ghrelin-induced food intake. (A) Two-hour food intake (mean ± SEM) of free-feeding rats after single administration of ghrelin IV (0.01–10 nmol). *P < vs. control vehicle. (B) Food intake of rats with bilateral subdiaphragmatic or gastric branch vagotomy after single administration of ghrelin IV (1.5 and 5 nmol). Control rats underwent sham operation. *P < (C) Food intake of rats with perivagal capsaicin application after single administration of ghrelin IV (1.5 and 5 nmol). *P < vs. control. (D) Food intake of rats with subdiaphragmatic vagotomy after single ICV administration of ghrelin (200 pmol). *P < (E) Food intake of rats with perivagal capsaicin application after single ICV administration of ghrelin (200 pmol). *P < □, saline; ■, ghrelin.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

3. Fig. 2
Effect of capsaicin treatment or vagotomy on ghrelin-induced GH secretion. (A, B) Time courses of plasma GH concentration (mean ± SEM) after administration of ghrelin IV to rats with (A) perivagal capsaicin application and (B) bilateral subdiaphragmatic vagotomy. (C, D) Time courses of plasma GH concentration after administration of GHRH IV to rats with (C) perivagal capsaicin application and (D) gastric branch vagotomy. *P < 0.01; **P < vs. control. A and C: ●, control; ○, capsaicin; B and D: ●, control; ○, vagotomy.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

4. Fig. 3
Localization of Fos expression in response to administration of ghrelin IV to rats that received capsaicin treatment or sham operation. (A) Fos is found in neurons of the arcuate nucleus of sham-operated rats. Costaining of (B) Fos (blue-black) and NPY neurons (brown) and (C) GHRH neurons (brown) in the arcuate nucleus of sham-operated rats. (D) No Fos expression is seen in response to ghrelin in capsaicin-treated rats. 3v, third ventricle. Scale bars: A, D, 100 μm; B, C, 50 μm.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

5. Fig. 4
Expression of ghrelin receptor mRNA in vagal nodose ganglion and binding of 125I-ghrelin in the vagus nerve. (A) Representative electrophoretic analysis patterns of RT-PCR products of ghrelin receptor mRNA in the nodose ganglion and hypothalamus of rats. (B) Photomicrograph of the nodose ganglion stained with H&E to visualize its cytoarchitecture. (C, D, and E) In situ hybridization for ghrelin receptor mRNA. (C) Hybridization signals on the nodose ganglion (red). (D) No hybridization signals are seen on the nodose ganglion after addition of an excess of unlabeled probes. (E) Bright-field photomicrograph of liquid emulsion autoradiography. Positive signals are present on cell bodies. Scale bars: B, C, and D, 500 μm; E, 100 μm. (F) Representative autoradiograph showing binding sites of 125I-ghrelin in the vagus nerve. (G) Accumulation of 125I-ghrelin binding sites around the ligation of the vagus nerve. Binding of 125I-ghrelin is abolished by addition of an excess of ghrelin. Values along the abscissa indicate distance (mm) from the ligature. Negative values correspond to areas proximal to the ligature and positive values correspond to areas distal to the ligature. Data are expressed as mean ± SEM (n = 5). *P < 0.02; **P < vs. distal 2 mm. (G) ●, 125I-ghrelin; ○, cold excess.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

6. Fig. 5
Effects of administration of ghrelin IV, des-acyl ghrelin, and CCK on gastric vagal afferent discharge. (A) Ghrelin, (B) but not des-acyl ghrelin, suppresses gastric vagal afferent activity. *P < 0.001; **P < vs. value at 0 minutes. (C) Stimulative effect of CCK on the gastric vagal afferent activity. *P < 0.05; **P < vs. value at 0 minutes. Representative data of gastric vagal afferent discharge rates are shown in the upper figures. Vertical bar: 100 impulses/5 sec; horizontal bar: 30 minutes.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions