Recent reports have provided evidence of a link between the endogenous brain cannabinoid system and the endogenous central opioid systems. Here we report that the selective CB1 receptor antagonist SR 141716A induced behavioral and endocrine alterations associated with opiate withdrawal in morphine-dependent animals in a dose-dependent manner and that naloxone induced an opiate withdrawal syndrome in animals made cannabinoid-dependent by repeated administration of the potent cannabinoid agonist HU-210. Additionally CB1 and mu-opioid receptor mRNAs were co-localized in brain areas relevant for opiate withdrawal such as the nucleus accumbens, septum, dorsal striatum, the central amygdaloid nucleus and the habenular complex. These results suggest that CB1 cannabinoid receptors may play a role in the neuroadaptive processes associated with opiate dependence, and they lend further support for the hypothesis of a potential role of cannabinoid receptors in the neurobiological changes that culminate in drug addiction.
We have studied the effect of chronic noise stress (St) and ACTH administration (Ac) affecting blood pressure and plasma corticosterone levels in male Wistar rats. Both chronic treatments elicited an increase in plasma corticosterone and blood pressure levels. The blood pressure increased from the first week of treatment period in St and Ac rats and remained high 4 weeks after the end of the stress period. However, blood pressure elevation decrease progressively during the first three weeks of post-treatment in ACTH administrated rats. The rise of blood pressure levels was due to the effect of chronic treatment. This was demonstrated by the absence of differences between the two values of blood pressure measurement with and without daily treatment in both St and Ac groups. Increased corticosterone levels decreased rapidly during the post-treatment period in St and Ac rats. The results suggest a possible relationship between the development of hypertension and the Hypothalamus-Hypophysis-adrenal (HHA) axis stimulation in rats.
Endocrine side effects of the immunosuppressive drug cyclosporine (CyA) include changes in anterior pituitary hormone secretion. The aim of the present study was to examine the effects of CyA on the responsiveness of in situ and ectopic anterior pituitary prolactin (PRL), growth hormone (GH) and luteinizing hormone (LH) release response to dopamine (DA) and thyrotropin-releasing hormone (TRH) treatment in young female rats, and to evaluate the possible PRL participation in these effects. Thirty day old rats were rendered hyperprolactinemic by transplanting an anterior pituitary gland of a littermate donor, under the kidney capsule, and were then injected with CyA or vehicle for 2 or 8 days. Sham-operated rats were used as controls and treated in the same way. CyA treatment prevented the increase in plasma PRL levels which occurred in controls after pituitary grafting. In vitro basal PRL release of in situ pituitaries from either sham-operated and/or pituitary-grafted animals was decreased by CyA treatment at any point studied. Basal in vitro secretion of GH was only decreased in the in situ pituitaries from grafted animals after 2 days of CyA therapy. The presence of an ectopic pituitary lead to an increase in the in vitro basal LH secretion from in situ pituitaries as compared to those from sham-operated rats. Basal LH release rates were not changed by CyA treatment, although the LH release in vitro did increase in the in situ pituitaries from sham-operated animals treated with the drug for 2 days. DA addition to the incubation media decreased the in vitro release of PRL, GH and LH from the in situ pituitaries of sham-operated and pituitary-grafted animals treated with vehicle. In CyA treated animals, DA decreased in vitro PRL release from the in situ pituitaries of animals, independently of the presence or absence of an ectopic pituitary. Reductions of the in vitro GH and LH release release after DA treatment were higher in the in situ pituitaries from grafted animals on day 8 of CyA or vehicle treatment. TRH increased the in vitro release of the three hormones with differential effects related to the length of the treatment with CyA and/or the presence of an ectopic pituitary. In vitro release of PRL and GH by ectopic pituitaries was inhibited by previous treatment with CyA and this effect was decreased proportional to the duration of the treatment with the drug, while LH secretion was not modified. Addition of DA to the incubation media resulted in a marked reduction of in vitro PRL and GH release, but only at day 8 of vehicle treatment on GH release did DA addition to media further decrease the release of both hormones from ectopic pituitaries from animals treated for 2 or 8 days with the drug, whereas LH secretion was not modified. TRH addition to the incubation media of ectopic pituitaries surprisingly reduced PRL and GH secretion on day 8 of CyA treatment or after surgery. The results of these studies suggest that CyA can act directly at the hypophyseal level modifying pituitary responsiveness to external...
Melatonin (100 micrograms/rat) was administered to female rats on day 5 of life, 3 hours prior to the onset of darkness or at 12:00 hours. Melatonin administration induced precocious puberty in both cases, as indicated by the advance of the time of the vaginal opening and the appearance of the first estrous smear as compared with controls (P less than 0.01), together with an increase in the number of estrous smears (P less than 0.05) and a reduction in the number of diestrous smears (P less than 0.05). Decreased serum prolactin levels were observed on day 21 of age (P less than 0.05) in melatonin-treated rats with both of the melatonin injection times as compared with controls. No differences were apparent in basal luteinizing hormone (LH) levels either at 30 or at 60 days of age comparing melatonin- and vehicle-treated rats with either of the scheduled melatonin injection times. As to serum follicle-stimulating levels (FSH) levels, there was a marked decrease in circulating FSH levels in melatonin-treated rats in both cases on days 21, 30, and 45 (P less than 0.05) as compared with controls. A marked increase of serum prolactin at both 48 and 55 hours after estradiol benzoate (EB) administration was detected in 30-day-old melatonin-treated rats as compared with controls (P less than 0.05 for both points). Also, an increased responsiveness of prolactin to EB was found on the first day post-administration. At 60 days of age, an increase in prolactin responses to EB was observed on the first day post-administration (31 and 48 hours after, (P less than 0.01), whereas no differences were detected at any other studied time. The LH burst that occurs 31 hours after EB administration in 30-day-old rats was decreased in melatonin-treated animals as compared with controls (P less than 0.05). In 60-day-old melatonin-treated rats, a marked increase in the LH response to EB administration, 31 hours after injection (P less than 0.01), was observed. These data suggest that neonatal melatonin administration in pharmacological amounts induces precocious puberty as measured by vaginal opening and, furthermore, it advances the appearance of the first estrous smear with age-dependent modifications of estrous cyclicity and prolactin and LH responses to EB.
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