SERUM PROLACTIN RESPONSE TO ETHER STRESS IN DIABETIC RATS - OPIATE SYSTEM CONTRIBUTION

Diabetes in streptozotocin-treated rats is associated with alterations in various neuroendocrine systems, including endogenous opioids. Thes e changes are suggested to be responsible for the significant reductio n in serum prolactin (PRL) response to a brief restraint stress in dia betic male rats, as compared with normoglycemic controls. The present study examines serum PRL response to ether exposure in diabetic male r ats. The animals' response to ether stress, which is known to be relat ed 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 a nd 7 after surgery in a group of rats which were pretreated with naltr exone (Nalt), an opioid receptor antagonist. Opioid receptor sensitiza tion 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 si gnificant 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 r ecorded in the diabetic rats. Opioid receptor blockade by Halt adminis tration 30 min before ether exposure eliminated this difference. Opioi d receptor sensitization by morphine pretreatment facilitated PRL secr etion in normoglycemic rats exposed to ether, while no effect could be distinguished in the diabetic group. It is therefore concluded that t he streptozotocin-induced diabetic rats do not differ from normoglycem ic ones in their ability to respond to acute ether stress by itself. H owever, enhanced PRL secretion induced by ether exposure under additio nal surgical stress, or by presensitization of the opioid receptors by morphine, is prevented in diabetic rats, probably due to diminished o pioid receptor response.