Abstract
The formation of gastric stress ulcers was studied as a function of interactions between thyrotropin releasing hormone (TRH) and endogenous opioids in the central amygdalar nucleus (CEA) in rats. Bilateral microinjections of TRH (1 or 10 μg) into the CEA produced dose-related aggravations in cold restraint stress (CRS, 3 h at 4°C) — induced gastric ulcer formation. Similar stress ulcer facilitating effects were also seen with intra-CEA injections of the opioid antagonist, naloxone (1 or 10 μg). On the other hand, the enkephalin analog, d-Ala 2-metenkephalinamide (DAMEA, 1, 10 or 20 μg) produced dose-dependent attenuations in gastric stress pathology, the effects being most marked with the latter two doses. Pretreatment of rats with intra-CEA naloxone (1 μg) (a) antagonized the gastric cytoprotective effects of DAMEA (20 μg) and (b) further aggravated the ulcerogenic response of TRH (1 μg), without influencing significantly the TRH (10 μg) effect. Further, when DAMEA (20 μg) was administered intra-CEA just after TRH (10 μg), the stress ulcer facilitating effects of the latter was neutralized. The results indicate that TRH-enkephalin interactions are possible at the level of the CEA during CRS-induced gastric ulcer formation.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
