Anorexigenic effects of pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal peptide in the chick brain are mediated by corticotrophin-releasing factor.
Intracerebroventricular (ICV) injection of pituitary adenylate cyclase-activating polypeptide-38 (PACAP) or vasoactive intestinal peptide (VIP) inhibits feeding in chicks. However, the underlying anorexigenic mechanism(s) has not yet been investigated. The present study investigated whether these peptides influence the activity of corticotrophin-releasing factor (CRF) neural pathways in the brain of chicks. Firstly, we found that ICV injections of PACAP and VIP increased plasma corticosterone concentrations. The corticosterone-releasing effect of PACAP was completely attenuated by co-injection of astressin, a CRF receptor antagonist, but this effect was only partial for VIP. These results demonstrated that CRF neurons mediate the actions of PACAP and, to a lesser extent, VIP, and suggest that the signaling mechanisms differ between the two peptides. This difference may arise from the two peptides interacting with different receptors because the corticosterone-releasing effect of PACAP, but not VIP, was completely attenuated by co-injection of PACAP (6-38), a PACAP receptor antagonist. Finally, we examined the effect of ICV co-injection of astressin on the anorexigenic effects of PACAP and VIP and found that the effects of both peptides were attenuated by astressin. Overall, the present study suggests that the anorexigenic effects of PACAP and VIP are mediated by the activation of CRF neurons.
Tachibana
Tetsuya
T
Laboratory of Advanced Animal and Marine Bioresources, Graduate School of Bioresource and Bioenvironmental Science, Kyushu University, Fukuoka 812-8581, Japan. tetsu@brs.kyushu-u.ac.jp
Saito
Ei-Suke
ES
Takahashi
Hirokazu
H
Saito
Shin
S
Tomonaga
Shozo
S
Boswell
Tim
T
Furuse
Mitsuhiro
M
D000818:Animals; D000831:Animals, Newborn; D000855:Anorexia / Q000378:metabolism / Q000473:pathology*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D003345:Corticosterone / Q000097:blood; D003346:Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000494:pharmacology; D004435:Eating / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D007276:Injections, Intraventricular; D008297:Male; D009474:Neurons / Q000187:drug effects; D009479:Neuropeptides / Q000494:pharmacology*; D018696:Neuroprotective Agents / Q000494:pharmacology; D010446:Peptide Fragments / Q000494:pharmacology; D051219:Pituitary Adenylate Cyclase-Activating Polypeptide; D018019:Receptors, Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors; D051236:Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide; D011979:Receptors, Pituitary Hormone / Q000037:antagonists & inhibitors; D018005:Receptors, Vasoactive Intestinal Peptide / Q000037:antagonists & inhibitors; D015398:Signal Transduction; D013552:Swine; D014660:Vasoactive Intestinal Peptide / Q000494:pharmacology*
C495401:ADCYAP1 protein, human; D009479:Neuropeptides; D018696:Neuroprotective Agents; D010446:Peptide Fragments; D051219:Pituitary Adenylate Cyclase-Activating Polypeptide; D018019:Receptors, Corticotropin-Releasing Hormone; D051236:Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide; D011979:Receptors, Pituitary Hormone; D018005:Receptors, Vasoactive Intestinal Peptide; C104416:astressin; D014660:Vasoactive Intestinal Peptide; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone