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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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- Cantero-Garcia, N, et al.
(författare)
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The Combination of Galanin (1-15) and Escitalopram in Rats Suggests a New Strategy for Alcohol Use Disorder Comorbidity with Depression
- 2022
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Ingår i: Biomedicines. - : MDPI AG. - 2227-9059. ; 10:2
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Tidskriftsartikel (refereegranskat)abstract
- Alcohol use disorder (AUD) is highly prevalent, and over 50% of AUD patients also suffer major depressive disorders. Selective 5-HT reuptake inhibitors (SSRIs) can reduce rodent ethanol drinking but exert modest clinical efficacy in alcoholic individuals. Finding new pharmacological strategies that could modulate alcohol consumption and depression is necessary. We have analyzed the effect of Galanin (1–15) [GAL(1–15)] on escitalopram (ESC)-mediated effect in alcohol consumption using the alcohol self-administration test, the nuclei involved in the effect, and whether GAL(1–15) + ESC modulated the response in despair or anxiety tests in animals under chronic alcohol intake. GAL(1–15) + ESC combination substantially reduced alcohol intake in the alcohol self-administration test and, moreover, enhanced the reduction of reward capacity of ESC on different reinforcers such as sucrose or saccharine. GAL(1–15) + ESC coadministration significantly decreases the number of C-Fos-IR TH cell bodies in the VTA, and PCA analysis suggests that one functional network, including VTA, RMTg and DR, is involved in these effects. Significantly in rats with chronic alcohol consumption, GAL(1–15) reversed adverse ESC-mediated effects in the depression-related behavioural test and forced swimming test. The results open up the possibility of using GAL(1–15) in combination with the SSRI Escitalopram as a novel strategy in AUD comorbidity with depression.
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