The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Gastric distension enhances CCK- induced Fos-like immunoreactivity in the dorsal hindbrain by activating 5-HT3 receptors.

The combination of gastric distension and cholecystokinin (CCK) enhances both suppression of food intake and induction of c-Fos-like immunoreactivity (Fos-LI) in the dorsal vagal complex (DVC). Previously, we have shown that serotonin type-3 (5-HT3) receptor mediation of suppression of food intake by CCK requires gastric participation. Therefore, we hypothesized that 5-HT3 receptors mediate CCK-induced Fos-LI in the dorsal hindbrain through a mechanism that involves gastric distension. To test this hypothesis, we counted Fos-LI in the DVC of ondansetron (1 mg/kg; 5-HT3 receptor antagonist) and vehicle-treated rats following gastric balloon distension (5 ml), CCK (1 microg/kg) administration, or CCK combined with gastric distension. Ondansetron administration attenuated DVC Fos-LI by CCK administration. Likewise, ondansetron attenuated Fos-LI by gastric distension in the DVC, specifically within the nucleus of the solitary tract (NTS) and area postrema (AP) nuclei. The most pronounced attenuation of distension-induced Fos-LI by ondansetron occurred in the NTS, particularly in the medial and intermedial NTS. When combined, CCK and gastric distension enhanced Fos-LI in the DVC greater than each treatment alone. Furthermore, ondansetron administration attenuated the overall DVC enhanced Fos-LI induced by CCK + gastric distension, in particular at the NTS and AP nuclei. We found that, within the mid-to-caudal regions of the NTS and AP, 5-HT3 receptors most significantly mediate neuronal activation by CCK + distension. In conjunction with previous behavioral data, these results show that gastric distension enhances CCK- induced neuronal activation in the DVC by activating 5-HT3 receptors.[1]

References

 
WikiGenes - Universities