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- Diaz-Cabiale, Z, et al.
(författare)
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Oxytocin/alpha(2)-Adrenoceptor interactions in feeding responses
- 2000
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Ingår i: Neuroendocrinology. - : S. Karger AG. - 0028-3835 .- 1423-0194. ; 71:3, s. 209-218
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Tidskriftsartikel (refereegranskat)abstract
- The modulation of α<sub>2</sub>-adrenoceptor-induced food intake by oxytocin has been evaluated in studies on food intake and by quantitative receptor autoradiography in the hypothalamus and the amygdala of the rat. The effects of lateral intracerebroventricular administration of clonidine and oxytocin were evaluated on food intake in satiated animals. Food consumption was measured at 30, 90, 240 min and 22 h (1,320 min) after injection. The coinjection of oxytocin and clonidine was found to counteract the increase in food intake produced by clonidine (p < 0.001) in satiated rats. Receptor autoradiographic experiments showed that oxytocin significantly increased the K<sub>d</sub> values of [<sup>3</sup>H]<i>p</i>-aminoclonidine α<sub>2</sub>-agonist-binding sites in the hypothalamus. Effective oxytocin concentrations ranged between 0.3 and 1 n<i>M</i> (p < 0.05) with a maximal action of 250% at 1 n<i>M</i>. The B<sub>max</sub> value was significantly increased (p < 0.05) for all concentrations of oxytocin. In the amygdala, oxytocin also increased both the K<sub>d</sub> of [<sup>3</sup>H]<i>p</i>-aminoclonidine-binding sites by about 190% at 1 n<i>M</i> and the B<sub>max</sub> values at 1 and 3 n<i>M</i> (p < 0.05). Oxytocin (1 n<i>M</i>) also significantly and substantially (p < 0.01) increased the K<sub>d</sub> and B<sub>max</sub> values of the [<sup>3</sup>H]UK 14.304 α<sub>2</sub>-agonist-binding sites in the hypothalamus and amygdala in agreement with the results obtained with the other agonist of the α<sub>2</sub>-adrenoceptor [<sup>3</sup>H]<i>p</i>-aminoclonidine. This effect was partially blocked by the presence of the specific oxytocin receptor antagonist, CAP. These findings suggest the existence of an antagonistic oxytocin/α<sub>2</sub>-receptor interaction in the hypothalamus and amygdala that may be of relevance for the demonstrated modulation of α<sub>2</sub>-adrenoceptor-induced feeding responses by oxytocin.
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- Petersson, M, et al.
(författare)
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Long-term changes in gastrin, cholecystokinin and insulin in response to oxytocin treatment
- 1999
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Ingår i: Neuroendocrinology. - : S. Karger AG. - 0028-3835 .- 1423-0194. ; 69:3, s. 202-208
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Tidskriftsartikel (refereegranskat)abstract
- The present study was designed to investigate how repeated injections of oxytocin influence plasma levels of vagally controlled hormones such as gastrin, cholecystokinin (CCK), insulin and somatostatin, as well as of endogenous oxytocin and glucose. Since oxytocin may enhance the activity of centrally located α<sub>2</sub>-adrenoreceptors, a second aim of this study was to explore whether these receptors are involved in the effects. For this purpose, oxytocin (1.0 mg/kg) or NaCl was given subcutaneously (s.c.) once a day during 5 days to male rats. Rats were decapitated 1, 3 and 10 days after the last injection, blood was collected and hormone levels were radioimmunoassayed. The oxytocin treatment caused an elevation of plasma levels of oxytocin 1 day (p < 0.05) but not 3 and 10 days after treatment. Gastrin levels were decreased on day 1, 3 and 10 (ANOVA; p < 0.01). In addition, both insulin and CCK levels were decreased in response to the oxytocin treatment when measured 3 and 10 days after the last injection (ANOVA; insulin p < 0.01, CCK p < 0.05). When the α<sub>2</sub>-adrenoreceptor agonist clonidine (2.5 µg/kg intracerebroventricularly) was administered 3 days after the 5-day treatment period with oxytocin or saline, plasma levels of insulin and CCK increased significantly (p < 0.05) in the oxytocin-treated rats, when compared to saline-treated controls receiving clonidine only. No change in glucose or somatostatin levels was found in response to the oxytocin treatment. In conclusion, these results show that oxytocin induces long-lasting changes in plasma levels of gastrin, CCK and insulin, without affecting somatostatin or glucose levels. These effects may be mediated by changes in vagal nerve activity.
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