Comparison of Fos induced in rat brain by GLP-1 and amylin

Rowland, Neil E.; Crews, Emily; Gentry, Rachel M

doi:10.1016/s0167-0115(97)01034-3

Cited by 107 publications

(88 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2D), NTS, LPB, Ce and BSTL, . This is consistent with results from previous studies (Rowland et al, 1997;Riediger et al, 2004) demonstrating amylin-induced activation in these brain areas.…”

Section: Projections To Dlhasupporting

confidence: 93%

“…Immunohistochemical studies using the immediate early gene product c-Fos as a marker of neuronal activation showed that peripherally applied amylin not only activates the AP, but also the nucleus of the solitary tract (NTS), the lateral parabrachial nucleus (LPB), the central amygdaloid nucleus (Ce) and the lateral subdivisions of the bed nucleus of the stria terminalis (BSTL) (Rowland et al, 1997;Riediger et al, 2004). These brain structures are part of the central gustatory/enteroceptive systems and are mutually interconnected and linked to the hypothalamus, the main integrative centre for the control of energy balance (Saper, 2002).…”

Section: -Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Identification of central projections from amylin-activated neurons to the lateral hypothalamus

2010

View full text Add to dashboard Cite

The ability of the pancreatic hormone amylin to inhibit food intake relies on a direct activation of the area postrema (AP). This activation is synaptically transmitted to the nucleus of the solitary tract (NTS), the lateral parabrachial nucleus (LPB), the central amygdaloid nucleus (Ce) and the lateral bed nucleus of stria terminalis (BSTL). Interestingly, neurons of the rostro-dorsal lateral hypothalamic area (dLHA), which are activated during fasting, are inhibited by peripheral amylin, although they lack amylin receptors. Using the retrograde tracer cholera toxin-B (Ctb) we analyzed whether the dLHA receives neuronal projections from amylin-activated brain areas. The anterograde tracer biotinylated dextran-amine (BDA) was used to confirm the projections and to identify further neuronal pathways potentially involved in amylin signaling. We identified dense projections from the amylin activated neurons in the LPB and sparse projections from the NTS to the dLHA. LPB fiber efferents were found in close proximity to dLHA nuclei activated by 24h of fasting. The AP and the Ce showed no projections to the dLHA. Dense efferents were also observed from the LPB to other hypothalamic areas, namely to the ventromedial, dorsomedial, paraventricular and arcuate nuclei. This study provides neuroanatomical evidence that among the amylin activated areas, the LPB provides the strongest input to the dLHA, thus it may mediate the amylin-induced inhibition of the dLHA. ABSTRACTThe ability of the pancreatic hormone amylin to inhibit food intake relies on a direct

show abstract

Section: Projections To Dlhasupporting

confidence: 93%

Section: -Introductionmentioning

confidence: 99%

Identification of central projections from amylin-activated neurons to the lateral hypothalamus

2010

View full text Add to dashboard Cite

show abstract

“…Glucagon like Peptide-1 (GLP-1) is released in response to a meal from the small intestine [299] and reduces food-intake both in animals and humans [289, 300for review]. As a central site of action is possible [301][302][303], it is of interest that both GLP-1 and the GLP agonist exendin-4 stimulate 5-HT release from hypothalamic synaptosomes [304]. However, an icv injection of either one reduced hypothalamic 5-HT level.…”

Section: -Ht Interactions With Other Gastrointestinal Peptidesmentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

243

165

View full text Add to dashboard Cite

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...

show abstract

“…CCK-8S increases Fos expression in the PVN, DMH and NTS [23,25,29,33,38] while systemic or icv application of the long-term satiety signal leptin induces neuronal activation in PVN and DMH neurons [12,44], and peptide YY increases Fos expression in NTS, AP [6], and ARC [4]. Glucagonlike peptide 1 modulates the number of Fos-ir positive neurons in ARC [44], PVN, NTS and AP [28,39], and peripheral amylin leads to increased neuronal activation in the NTS and AP [39]. Another puzzling fact is the lack of evidence for in vivo synthesis of obestatin [13].…”

Section: Discussionmentioning

confidence: 99%

Peripheral obestatin has no effect on feeding behavior and brain Fos expression in rodents

et al. 2008

View full text Add to dashboard Cite

Obestatin is produced in the stomach from proghrelin by post-translational cleavage. The initial report claimed anorexigenic effects of obestatin in mice. Contrasting studies indicated no effect of obestatin on food intake (FI). We investigated influences of metabolic state (fed/fasted), environmental factors (dark/light phase) and brain Fos response to intraperitoneal (ip) obestatin in rats, and used the protocol from the original study assessing obestatin effects in mice. FI was determined in male rats injected ip before onset of dark or light phase, with obestatin (1 or 5 μmol/kg), CCK8S (3.5 nmol/kg) or 0.15 M NaCl, after fasting (16 h, n = 8/group) or ad libitum (n = 10-14/group) food intake. Fos expression in hypothalamic and brainstem nuclei was examined in freely fed rats 90 min after obestatin (5 μmol/kg), CCK8S (1.75 nmol/kg) or 0.15 M NaCl (n = 4/group). Additionally, fasted mice were injected ip with obestatin (1 μmol/kg) or urocortin 1 (2 nmol/kg) 15 min before food presentation. No effect on FI was observed after obestatin administration during the light and dark phase under both metabolic conditions while CCK8S reduced FI irrespectively of the conditions. The number of Fos positive neurons was not modified by obestatin while CCK8S increased Fos expression in selective brain nuclei. Obestatin did not influence the refeeding response to a fast in mice, while urocortin was effective. Therefore, peripheral obestatin has no effect on FI under various experimental conditions and did not induce Fos in relevant central neuronal circuitries modulating feeding in rodents.

show abstract

Comparison of Fos induced in rat brain by GLP-1 and amylin

Cited by 107 publications

References 16 publications

Identification of central projections from amylin-activated neurons to the lateral hypothalamus

Identification of central projections from amylin-activated neurons to the lateral hypothalamus

Serotonin controlling feeding and satiety

Peripheral obestatin has no effect on feeding behavior and brain Fos expression in rodents

Contact Info

Product

Resources

About