Appetite suppression by commonly used drugs depends on 5-HT receptors but not on 5-HT availability

Curzon, G.; Gibson, E.L.; Oluyomi, A.O.

doi:10.1016/s0165-6147(96)01003-6

Cited by 142 publications

(75 citation statements)

References 41 publications

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“…Furthermore, the SB 242,084-induced reversal of this effect suggests it is mediated via increased stimulation of 5-HT 2C receptors. The d-fenfluramine-induced attenuation of cue reinstatement is also likely mediated by an increase in 5-HT 2C receptor stimulation via increased 5-HT release (Rowland and Carlton, 1986;Leferrere and Wurtman, 1989), as well as direct 5-HT 2C agonist actions of the parent compound and its active metabolite (Curzon et al, 1997;Rothman and Baumann, 2002) since the effect is reversed by SB 242,084. This finding suggests that increased stimulation of 5-HT 2C receptors inhibits cue reinstatement of cocaine-seeking behavior.…”

Section: Discussionmentioning

confidence: 99%

Differential Roles of 5-HT Receptor Subtypes in Cue and Cocaine Reinstatement of Cocaine-Seeking Behavior in Rats

Burmeister

Lungren

Kirschner

et al. 2003

Neuropsychopharmacol

101

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The 5-HT indirect agonist, d-fenfluramine, attenuates cue reinstatement of extinguished cocaine-seeking behavior. To investigate the role of 5-HT receptor subtypes in this effect, we examined whether the attenuation is reversed by either a 5-HT 1A , 5-HT 2A/C , or 5-HT 2C receptor antagonist. We also examined the effects of the antagonists alone on both cue and cocaine-primed reinstatement. Rats that had been trained to press a lever for cocaine (0.75 mg/kg/0.1 ml, i.v.) paired with light and tone cues underwent daily extinction sessions during which responding had no consequences. We then examined the effects of WAY 100635 (0-1.0 mg/kg, s.c.), ketanserin (0-10.0 mg/kg, i.p.), or SB 242,084 (0-1.0 mg/kg, i.p.) with and without d-fenfluramine (1.0 mg/kg, i.p.) pretreatment on cue reinstatement. Subsequently, we examined the effects of the antagonists on cocaine-primed (7.5 or 15.0 mg/kg, i.p.) reinstatement. The 5-HT 1A antagonist, WAY 100635, failed to alter cue reinstatement, but attenuated cocaine reinstatement. Conversely, the 5-HT 2A/C antagonist, ketanserin, attenuated cue reinstatement, but failed to alter cocaine reinstatement. The 5-HT 2C -selective antagonist, SB 242,084, did not alter cue or cocaine reinstatement, but was the only drug that reversed the d-fenfluramine-induced attenuation of cue reinstatement. The findings suggest that stimulation of 5-HT 1A receptors plays a critical role in cocaine-primed, but not cue, reinstatement. Furthermore, 5-HT 2A and 5-HT 2C receptors may play oppositional roles in cue reinstatement. The SB 242,084 reversal of the d-fenfluramine attenuation suggests that stimulation of 5-HT 2C receptors inhibits cue reinstatement, whereas the ketanserin-induced attenuation of cue reinstatement suggests that decreased stimulation of 5-HT 2A receptors inhibits this behavior.

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Section: Discussionmentioning

confidence: 99%

Differential Roles of 5-HT Receptor Subtypes in Cue and Cocaine Reinstatement of Cocaine-Seeking Behavior in Rats

Burmeister

Lungren

Kirschner

et al. 2003

Neuropsychopharmacol

101

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“…However, genetic manipulation of the 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 7 binds to the 5-HT2C receptor and also reduces food intake. This led to the conclusion that direct 5-HT2C receptor activation contributes to the hypophagic effects of d-fenfluramine [66][67][68]. Both dl-fenfluramine and d-fenfluramine accelerate the BSS in the majority of studies conducted in mice or rats [59, [69][70][71][72][73].…”

Section: Brain 5-ht and Satietymentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

266

167

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Serotonin has been implicated in the control of satiety for almost four decades. Historically, the insight that the appetite suppressant effect of fenfluramine is linked to serotonin has stimulated interest in and research into the role of this neurotransmitter in satiety. Various rodent models, including transgenic models, have been developed to identify the involved 5-HT receptor subtypes. This approach also required the availability of receptor ligands of different selectivity, and behavioural techniques had to be developed simultaneously which allow differentiating between unspecific pharmacological effects of these ligands and 'true' 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 IntroductionWhat are the behavioural and physiological mechanisms that promote satiety? How is satiety defined? Satiety can be seen as a behavioural state which arises from food consumption and suppresses the initiation of eating for a particular period of time [1]. This description alone suggests a high degree of complexity as peripheral post-ingestive and post-absorptive signals need to be relayed to the brain where they are integrated with other signals to produce (or not) the behavioural state called satiety. The state of satiety is brought about a process called satiation, where sensory, cognitive and early post-ingestive mechanisms bring feeding to a halt and thus stopping a meal. Promoting satiation alone must not necessarily lead to reduced total food intake as the frequency of meals could be increased subsequently. Many peripheral and brain mechanisms have been identified that are involved in the expression satiety and it has been suggested that serotonin accelerates satiation and prolongs satiety [2]. In the following, we will review the role of serotonin in satiety in more detail 1 . The reader will see that, despite immense progress made during the last years, the field is still far from being resolved.As serotonin (5-Hydroxytryptamine; 5-HT) is a phylogenetically old neurotransmitter, various functions had time to evolve in different phyla, but maybe also in different species. 5-HT receptors exist in animal cells for millions of years and they are as old as adrenoreceptors ore some peptide receptors, possibly even older [5,6]. Even in invertebrates such as molluscs (Aplysia californica) and annelids (Hirudo medicinalis), 5-HT might functionally be related to food intake [7]. 5-HT is involved in feeding even in the honeybee where it has separate effects in the gut and in the insect brain [8]. In general, however, 5-HT seems rather to be involved in appetitive behaviours in invertebrates whereas it has more of a satiating effect in vertebrates [9]. In general, 5-HT neurons seem to be more extensively distributed throughout the body in lower animals than in higher animals including mammals where 5-HT neurones...

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“…1985;Parada et al, 1992;Curzon et al, 1997 . It is well-known that indirectly acting compounds, with different mechanisms of action, can profoundly influence this function.…”

Section: Introductionmentioning

confidence: 99%

Selective inhibition of amine oxidases differently potentiate the hypophagic effect of benzylamine in mice

Banchelli

Ghelardini

Raimondi

et al. 2001

European Journal of Pharmacology

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In mice deprived of food for 12 h, the i.c.v. or i.p. administration of benzylamine, a substrate common to both monoamine oxidase B and semicarbazide-sensitive benzylamine oxidases, dose-dependently inhibited feeding. This effect was significantly potentiated by selective monoamine oxidase A and B inhibition, suggesting that central monoamines, known to be substrates of these enzymes may be Ž . released. The i.p. administration of semicarbazide-sensitive benzylamine oxidase inhibitors, B24 3,5-ethoxy-4-aminomethylpyridine and ŽŽ . . MDL 72274 E -2-phenyl-3-chloroallylamine strongly potentiated the effect of i.p. but not i.c.v.-administered benzylamine. The hypophagic effect of benzylamine was evaluated following i.c.v. administration, in comparison with the effect of the sympathomimetic compound amphetamine or the K q channel blocker tetraethylammonium, as reference compounds. Our results make it possible to define benzylamine as a centrally acting hypophagic compound devoid of amphetamine-like motor stimulatory effects and point to a role of B24 and MDL 72274 as specific peripheral enhancers of the pharmacological effects of benzylamine. q

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Appetite suppression by commonly used drugs depends on 5-HT receptors but not on 5-HT availability

Cited by 142 publications

References 41 publications

Differential Roles of 5-HT Receptor Subtypes in Cue and Cocaine Reinstatement of Cocaine-Seeking Behavior in Rats

Differential Roles of 5-HT Receptor Subtypes in Cue and Cocaine Reinstatement of Cocaine-Seeking Behavior in Rats

Serotonin controlling feeding and satiety

Selective inhibition of amine oxidases differently potentiate the hypophagic effect of benzylamine in mice

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