Sucrose consumption increases naloxone-induced c-Fos immunoreactivity in limbic forebrain

Citation
Jd. Pomonis et al., Sucrose consumption increases naloxone-induced c-Fos immunoreactivity in limbic forebrain, AM J P-REG, 278(3), 2000, pp. R712-R719
Citations number
42
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
278
Issue
3
Year of publication
2000
Pages
R712 - R719
Database
ISI
SICI code
0363-6119(200003)278:3<R712:SCINCI>2.0.ZU;2-9
Abstract
Opioids have long been known to have an important role in feeding behavior, particularly related to the rewarding aspects of food. Considerable behavi oral evidence suggests that sucrose consumption induces endogenous opioid r elease, affecting feeding behavior as well as other opioid-mediated behavio rs, such as analgesia, dependence, and withdrawal. In the present study, ra ts were given access to a 10% sucrose solution or water for 3 wk, then they were injected with 10 mg/kg naloxone or saline. Brains were subsequently a nalyzed for c-Fos immunoreactivity (c-Fos-IR) in limbic and autonomic regio ns in the forebrain and hindbrain. Main effects of sucrose consumption or n aloxone injection were seen in several areas, but a significant interaction was seen only in the central nucleus of the amygdala and in the lateral di vision of the periaqueductal gray. In the central nucleus of the amygdala, naloxone administration to those rats drinking water significantly increase d c-Fos-IR, an effect that was significantly enhanced by sucrose consumptio n, suggesting an upregulation of endogenous opioid tone in this area. The d ata from this study indicate that the central nucleus of the amygdala has a key role in the integration of gustatory, hedonic, and autonomic signals a s they relate to sucrose consumption, if not to food intake regulation in g eneral. Furthermore, the data from this study lend further support to the h ypothesis that sucrose consumption induces the release of endogenous opioid s.