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. 2001 May;73(1-2):223-7.
doi: 10.1016/s0031-9384(01)00467-x.

The differential effects of intravenously administered 8-OH-DPAT on operant food intake in satiated and food-deprived pigs are mediated by central 5-HT(1A) receptors

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The differential effects of intravenously administered 8-OH-DPAT on operant food intake in satiated and food-deprived pigs are mediated by central 5-HT(1A) receptors

I S Ebenezer et al. Physiol Behav. 2001 May.

Abstract

It has previously been shown that the intravenous administration of the 5-HT(1A) receptor agonist, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), increases food intake in satiated pigs and decreases food intake in fasted pigs. The present experiments were conducted to investigate the effects of central administration of the 5-HT(1A) receptor antagonist, N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]-N-2-pyridinyl-cyclohexane carbox-amide maleate (WAY 100635), on the stimulant and depressant effects of 8-OH-DPAT on operant food intake in satiated and hungry pigs. In Experiment 1, 8-OH-DPAT (25 microg/kg) produced an increase in operant feeding during the first 30 min following intravenous administration to satiated pigs. The 8-OH-DPAT-induced hyperphagia was completely abolished by pretreatment with WAY 100635 (0.3 mg) administered by intracerebroventricular injection. In Experiment 2, 8-OH-DPAT (25 microg/kg) administered intravenously 15 min prior to the onset of feeding in pigs that had been fasted for 22.5 h produced a decrease in operant food intake, which was most apparent during the first 30 min of the feeding period. The hypophagic effect was completely abolished by pretreatment with WAY 100635 (0.3 mg icv) administered 30 min before the start of the feeding period. In both experiments, WAY 100635 (0.3 mg icv) did not have any significant effects on feeding. The results of the present study extend previous results in the pig and show that both the hyperphagic and the hypophagic effects of 8-OH-DPAT in satiated and fasted pigs, respectively, are mediated by central 5-HT(1A) receptors.

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