A comparison of the effects of tryptamine and 5-hydroxytryptamine on feeding following injection into the paraventricular nucleus of the hypothalamus

doi:10.1016/0091-3057(89)90057-9

Pharmacology Biochemistry and Behavior

Volume 32, Issue 4, April 1989, Pages 907-911

https://doi.org/10.1016/0091-3057(89)90057-9 Get rights and content

Abstract

The effects of 5-hydroxytryptamine (5-HT) and tryptamine injected into the paraventricular nucleus of the hypothalamus (PVN) on food intake, and on noradrenaline- (NA) induced feeding were examined. In nondeprived rats, 12.5–100 nmol 5-HT reduced the intake of palatable wet mash diet over a 30-minute period. Tryptamine (50 and 100 nmol) was without effect in this paradigm. However, when tryptamine was injected into the PVN of rats pretreated with the monoamine oxidase inhibitor, pargyline, a strong anorectic effect was observed. The action of tryptamine in pargyline-treated rats was not affected by depletion of 5-HT levels in the PVN with PCPA. This indicates that the effect of tryptamine is not mediated by a release of endogenous 5-HT. Tryptamine injected into the PVN potentiated the effect of a low dose of 5-HT on food intake. This effect may be due to a prolongation of the activity of 5-HT resulting from tryptamine competing with 5-HT for the same reuptake system. Tryptamine and 5-HT attenuated the feeding response elicited by injection of 25 nmol NA into the PVN. Both tryptamine and 5-HT were more potent at attenuating the effects of NA than in reducing the intake of the palatable wet mash diet. Overall, the results suggest that tryptamine may act via the serotonergic system in the PVN to affect food intake, but it is a weaker compound than 5-HT in this respect.

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Citation Excerpt :
Although involved in many physiological processes, one of the main effects of central serotonin is to inhibit feeding behavior (Simansky, 1996; Berthoud, 2002). In rodents, for example, central administration of 5-HT decreases food intake (Leibowitz, 1986; Fletcher and Paterson, 1989), whereas selective depletion of central 5-HT is associated with hyperphagia and increased body weight (Breisch et al., 1976; Waldbillig et al., 1981). Also in humans, serotonin depletion has been associated with increased feeding behavior (Weltzin et al., 1995), although 5HIAA, a 5-HT metabolite, was found to be significantly elevated in cerebrospinal fluid (CSF) of overweight subjects (Markianos et al., 2013).
It is evident that eating in misalignment with the biological clock (such as in shift work, eating late at night and skipping breakfast) is associated with increased risk for obesity and diabetes. The biological clock located in the suprachiasmatic nucleus dictates energy balance including feeding behavior and glucose metabolism. Besides eating and sleeping patterns, glucose metabolism also exhibits clear diurnal variations with higher blood glucose concentrations, glucose tolerance and insulin sensitivity prior to waking up. The daily variation in plasma glucose concentrations in rats, is independent of the rhythm in feeding behavior. On the other hand, feeding itself has profound effects on glucose metabolism, but differential effects occur depending on the time of the day. We here review data showing that a disturbed diurnal eating pattern results in alterations in glucose metabolism induced by a disrupted circadian clock. We first describe the role of central serotonin on feeding behavior and glucose metabolism and subsequently describe the effects of central serotonin on the circadian system. We next explore the interaction between the serotonergic system and the circadian clock in conditions of disrupted diurnal rhythms in feeding and how this might be involved in the metabolic dysregulation that occurs with chronodisruption.
Serotonin delivery into the ventromedial nucleus of the hypothalamus affects differently feeding pattern and body weight in obese and lean Zucker rats
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Aim: To determine if central serotonin (5-HT)-induced satiety is altered in obesity. Methods: Obese and lean Zucker rats received infusion of 5-HT (5 μg/0.5 μl/h) or saline into the ventromedial nucleus of the hypothalamus (VMN) for 2 weeks. Results: In lean rats, 5-HT decreased body weight (7%) and total food intake (15%) which was due to a decreased meal size during the dark phase. In obese rats, a decrease of food intake was also observed in the dark phase, but it was compensated by an increased food intake during the light phase, resulting in no significant changes of total food intake and body weight. In obese rats, meal number but not meal size was affected by 5-HT delivery. Body fat content was not affected by 5-HT in obese rats, while cessation of 5-HT delivery in lean rats resulted in 13% increase. Conclusion: Intra-VMN 5-HT in obese rats did not increase meal-associated satiety as it did in lean rats, but modulated hunger. These results show that the Zucker obese phenotype is characterized by VMN resistance to 5-HT, which may contribute to neurobiological mechanisms of increased meal size and food intake and may diminish anti-obesity effects of serotonergic anorexiants.
Feeding behavior after metergoline or GR-46611 injections into the paraventricular nucleus of the hypothalamus in the pigeon
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The present study examined changes in spontaneous behavior of free-feeding pigeons in response to local injections of metergoline (MET, an antagonist of 5-HT_1/2 receptors; 5, 10 and 20 nmol), GR-46611 (GR, a 5-HT_1B/1D agonist; 0.6 and 6 nmol) or vehicle into the paraventricular hypothalamic nucleus (PVN). When infused into the PVN, MET and GR promptly and reliably elicited feeding at their higher doses, without affecting drinking or non-ingestive behaviors (locomotion, exploration, preening, sleep) during the first hour after injection. Both GR- and MET-evoked ingestive responses were associated only with an increase in feeding duration, with no changes in latency to start feeding. In a second series of experiments, the effective doses of MET (20 nmol) and GR (6 nmol) were injected into other diencephalic areas. This exploratory study revealed that intense feeding responses to both MET and GR local injections are also observed in the n. medialis hypothalami posterioris and in the adjacent n. lateralis hypothalami posterioris (PMH/PLH complex, in the caudoventral hypothalamus) and in the n. magnocellularis preopticus (PPM, in the caudal preoptic region). The behavioral profiles associated with these hyperphagic responses were nucleus-specific: in the PMH/PLH, MET-induced feeding was accompanied by an increase in total feeding duration and by a reduction in the latency to start feeding, while ingestive responses evoked by MET in the PPM were associated only with an increase in feeding duration (similar to that observed in the PVN experiments). No ingestive effects were observed after intracerebroventricular (ICV, lateral ventricle) injections of MET (10, 30, 100 or 300 nmol), while ICV injections of GR (3, 15 or 30 nmol) increased feeding only at the higher dose [Da Silva RA, De Oliveira ST, Hackl LPN, Spilere CI, Faria MS, Marino-Neto J, Paschoalini MA. Ingestive behaviors and metabolic fuels after central injections of 5-HT_1A and 5-HT_1D/1B receptors agonists in the pigeon. Brain Res, 2004;1026:275–283]. These data indicate the presence of a tonic inhibitory influence on feeding behavior exerted by 5-HT afferents on these hypothalamic areas, and suggest that these inputs, possibly mediated by non-rodent-type 5-HT_1D/1B receptors, can affect both satiety and satiation mechanisms.
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We investigated the effect of chronic dexfenfluramine (DFEN) treatment on macronutrient selection in a three-choice diet paradigm using Sprague–Dawley rats. Baseline macronutrient intakes were measured for several days before the initiation of treatment. In Experiment 1, daily intraperitoneal injections of DFEN (1.5 mg/kg) or saline were administered 60 min before dark onset for 12 consecutive days and 24 h macronutrient intakes were measured. DFEN significantly reduced absolute fat intake (kcal) by 30% and relative fat intake (% of total energy) by 14% in animals that received dexfenfluramine treatment compared to controls over the 12-day period. Absolute carbohydrate intake was increased 24% compared to controls, but this difference was not significant. These changes in food intake resulted in a 10% lower total energy intake. Upon discontinuation of the drug, fat intake of the DFEN-treated rats rebounded to control levels within 24 h. In Experiment 2, rats were assigned to carbohydrate- or fat-preferring groups based on the ratio of their average daily carbohydrate to fat intake (kcal). All animals then received DFEN. During DFEN treatment, fat-preferring rats reduced their daily fat intake from 62 to 53% of total energy. The low baseline fat intake of carbohydrate-preferring rats was reduced even further by DFEN (from 24 to 15% of total energy). These corresponding effects of DFEN on macronutrient selection in both fat- and carbohydrate-preferring rats indicate that chronic DFEN treatment selectively suppressed fat intake independent of the preferred macronutrient diet.
Decreased intake of a liquid diet in nonfood-deprived rats following intra-PVN injections of GLP-1 (7-36) amide
1997, Pharmacology Biochemistry and Behavior
McMAHON, L. R. AND P. J. WELLMAN. Decreased intake of a liquid diet in nonfood-deprived rats following intra-PVN injections of GLP-1 [7]-36 amide. PHARMACOL BIOCHEM BEHAV 58(3) 673–677, 1997.—ICV administration of glucagon-like peptide-1 [7]-36 amide (GLP-1) dose dependently suppresses food intake in rats, and induces activation of c-fos within rat paraventricular hypothalamus (PVN). The present study sought to determine whether GLP-1 [7]-36 amide may act within the PVN by examining the effects of intra-PVN administration of GLP-1 [7]-36 amide on food intake in rats. Adult male rats (n = 11) were prepared with indwelling guide cannulae aimed at the PVN. Rats were allowed access to a palatable liquid diet (Ensure) and water during a daily 60-min test period with intakes measured every 15 min. Intra-PVN administration of GLP-1 [7]-36 amide (10, 50, 100, and 200 ng) did not alter latency to feed, but did suppress liquid diet intake over a 1-h testing period, as a function of dose. These results suggest that GLP-1 [7]-36 amide may act, in part, to suppress feeding through interactions with cells within the PVN.

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A comparison of the effects of tryptamine and 5-hydroxytryptamine on feeding following injection into the paraventricular nucleus of the hypothalamus

Abstract

Neuroscience

Neuropharmacology

Pharmacol. Biochem. Behav.

Pharmacol. Biochem. Behav.

Prog. Neurobiol.

Life Sci.

Neuropharmacology

Neuropharmacology

Biochem. Pharmacol.

Brain Res. Bull.

Pharmacol. Biochem. Behav.

An extra-fine assembly for intracerebral microinjection

J. Physiol. (Lond.)

The subcellular distribution of β-phenylethylamine, p-tyramine and tryptamine in rat brain

J. Neurochem.