title: Serum prolactin response to ether stress in diabetic rats: opiate system contribution.
abstract: Diabetes in streptozotocin-treated rats is associated with alterations in various neuroendocrine systems, including endogenous opioids. These changes are suggested to be responsible for the significant reduction in serum prolactin (PRL) response to a brief restraint stress in diabetic male rats, as compared with normoglycemic controls. The present study examines serum PRL response to ether exposure in diabetic male rats. The animals' response to ether stress, which is known to be related to the opioid system, was examined twice in each rat: shortly after cannula insertion (Day 1), and seven days later. In order to evaluate the opiate system involvement, the experiment was repeated on Day 1 and 7 after surgery in a group of rats which were pretreated with naltrexone (Nalt), an opioid receptor antagonist. Opioid receptor sensitization was also performed by prior acute morphine administration on Day 7 after cannulation surgery. Following adaptation to the cannulation, no difference in serum PRL response to ether stress was found between diabetic and normoglycemic rats. However, on Day 1 after surgery, a significant difference was found between the diabetic and control groups: the normoglycemic (control) group exposed to ether responded to the surgical stress by augmented serum PRL levels. This response was not recorded in the diabetic rats. Opioid receptor blockade by Nalt administration 30 min before ether exposure eliminated this difference. Opioid receptor sensitization by morphine pretreatment facilitated PRL secretion in normoglycemic rats exposed to either, while no effect could be distinguished in the diabetic group. It is therefore concluded that the streptozotocin-induced diabetic rats do not differ from normoglycemic ones in their ability to respond to acute ether stress by itself. However, enhanced PRL secretion induced by ether exposure under additional surgical stress, or by presensitization of the opioid receptors by morphine, is prevented in diabetic rats, probably due to diminished opioid receptor response.
authors.affiliation: Institute for the Study of Fertility, Tel Aviv Sourasky Medical Center, Serlin Maternity Hospital, Israel.
authors.forename: L
authors.initials: L
authors.lastname: Yogev
authors.forename: H
authors.initials: H
authors.lastname: Yavetz
authors.forename: A
authors.initials: A
authors.lastname: Gottreich
authors.forename: D
authors.initials: D
authors.lastname: Oppenheim
authors.forename: Z T
authors.initials: ZT
authors.lastname: Homonnai
authors.forename: G
authors.initials: G
authors.lastname: Paz
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000097:blood*; D004986:Ether / Q000633:toxicity*; D008297:Male; D009020:Morphine / Q000494:pharmacology; D009271:Naltrexone / Q000494:pharmacology; D009292:Narcotic Antagonists; D011388:Prolactin / Q000097:blood*; D051381:Rats; D017208:Rats, Wistar; D011957:Receptors, Opioid / Q000502:physiology*; D013312:Stress, Physiological / Q000097:blood* / Q000139:chemically induced
chemical_list: D001786:Blood Glucose; D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D004986:Ether; D009271:Naltrexone; D009020:Morphine; D011388:Prolactin