The 5-HT3 receptor ligand, [3H]BRL 43694, binds to presynaptic sites in the nucleus tractus solitarius of the rat

Pratt, Gerard D.; Bowery, Norman G.

doi:10.1016/0028-3908(89)90012-9

Cited by 142 publications

(34 citation statements)

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“…Several studies have demonstrated that 5-HT is able to modulate synaptic transmission at this first central vagal synapse via 5-HT 3 receptors present on vagal afferent terminals (28,37,75). In the rat, vagal afferent terminals within the NTS display some of the highest densities of 5-HT 3 receptors and play a prominent role in cardiovascular regulation (38,42,51,75). Activation of 5-HT 3 receptors within the NTS results in a rise in blood pressure (37,38) and inhibition of the bradycardia evoked by chemoceptor activation (38,59) as well as inhibition of the Bezold-Jarisch reflex (50,60).…”

Section: Discussionmentioning

confidence: 99%

“…5-HT 3 receptors are ubiquitous throughout the central and peripheral nervous systems, and the highest density of these receptors in the central nervous system is found within the dorsal vagal complex (21, 66). Many of these 5-HT 3 receptors are located on the nerve terminals of vagal afferent neurons since vagotomy was found to decrease 5-HT 3 receptor binding dramatically (41,42,51). The NTS receives a prominent serotonergic innervation from other brainstem nuclei, mostly notable the medullary raphe nuclei (64, 65, 69), although vagal afferent neurons themselves contain 5-HT (49, 67).…”

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confidence: 98%

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Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Wan

Browning²

2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Acute hyperglycemia has profound effects on vagally mediated gastrointestinal functions. We have reported recently that the release of glutamate from the central terminals of vagal afferent neurons is correlated directly with the extracellular glucose concentration. The present study was designed to test the hypothesis that 5-HT(3) receptors present on vagal afferent nerve terminals are involved in this glucose-dependent modulation of glutamatergic synaptic transmission. Whole-cell patch-clamp recordings were made from neurons of the nucleus tractus solitarius (NTS) in thin rat brainstem slices. Spontaneous and evoked glutamate release was decreased in a concentration-dependent manner by the 5-HT(3) receptor selective antagonist, ondansetron. Alterations in the extracellular glucose concentration induced parallel shifts in the ondansetron-mediated inhibition of glutamate release. The changes in excitatory synaptic transmission induced by extracellular glucose concentration were mimicked by the serotonin uptake inhibitor, fenfluramine. These data suggest that glucose alters excitatory synaptic transmission within the rat brainstem via actions on tonically active 5-HT(3) receptors, and the number of 5-HT(3) receptors on vagal afferent nerve terminals is positively correlated with the extracellular glucose concentration. These data indicate that the 5-HT(3) receptors present on synaptic connections between vagal afferent nerve terminals and NTS neurons are a strong candidate for consideration as one of the sites where glucose acts to modulate vagovagal reflexes.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Wan

Browning²

2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…This effect is largely relayed by the vagus to the NTS and mediated 16 by 5-HT3 receptors which are expressed on peripheral dendritic terminals of vagal afferents innervating the stomach [107,[204][205][206][207]. High densities of 5-HT3 receptor binding sites within the central nervous system have also been found in the NTS [208,209] and local administration of the 5-HT3 antagonist odansetron increased sucrose intake [107]. After intestinal anaphylaxis, increased c-fos staining was observed in the NTS, the parabrachial nucleus, and the hypothalamic PVN [210].…”

Section: Brain Mechanisms Of Serotonergic Satietymentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

257

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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“…After Kilpatrick et al (1987) first demonstrated the presence of [ 3 H]GR65630 binding sites in rat brain, the putative rat brain 5-HT3 receptor was characterized with the use of other different radioligands Pratt and Bowery 1989;Reynolds et a1. 1989;Schmidt et a1.…”

Section: Development Of Selective Drugs Active At the 5-ht3 Receptormentioning

confidence: 99%

The 5-HT3 Receptor in Mammalian Brain: A New Target for the Development of Psychotropic Drugs?

Apud

1993

Neuropsychopharmacol

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Serotonin (5-HT) is a neurotransmitter in the central nervous system (eNS) of vertebrates and invertebrates.In vertebrates, 5-HT participates in the regulation of var ious physiologic functions, including pain perception, blood pressure, sleep, homeothermia, and sexual ac ti vity. It is also believed that 5-HT may participate in the expression of symptoms of certain psychiatric dis orders, such as depression and anxiety. In this context, most of our knowledge concerning the participation of S-HT and 5-HT receptors in psychopathology has come from the characterization of the mechanisms of action of various drugs that are effective in relieving the symp toms of psychiatric disorders.That the 5-HT receptor population in the periph e ry might be heterogeneous was fIrst suggested by the earl y pioneering work of two independent groups (Rocha e Silva et a1. 1953; Gaddum and Hameed 1954).It was not until the late 1970s, however, that Peroutka and Snyder (1979) described, in the eNS, the existence of two diff erent 5-HT recognition sites labeled by lyser gic acid diethylamine, the serotonin-1 (5-HT1) and the serotonin-2 (5-HT2) binding sites. A third type of 5-HT receptor, the 5-HT3 recogni tion site, has also been identifIed (Fozard et a1.

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The 5-HT3 receptor ligand, [3H]BRL 43694, binds to presynaptic sites in the nucleus tractus solitarius of the rat

Cited by 142 publications

References 9 publications

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Serotonin controlling feeding and satiety

The 5-HT3 Receptor in Mammalian Brain: A New Target for the Development of Psychotropic Drugs?

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The 5-HT3 receptor ligand, [3H]BRL 43694, binds to presynaptic sites in the nucleus tractus solitarius of the rat

Cited by 142 publications

References 9 publications

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT3 receptors

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT3 receptors

Serotonin controlling feeding and satiety

The 5-HT3 Receptor in Mammalian Brain: A New Target for the Development of Psychotropic Drugs?

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Product

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Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors

Glucose increases synaptic transmission from vagal afferent central nerve terminals via modulation of 5-HT₃ receptors