5-hydroxy-L-tryptophan Suppressed Food Intake in Rats Despite an Increase in the Arcuate NPY Expression

Moon, Young-Hyun; Choi, Si Ho; Yoo, Sang Bae; Lee, Jong-Ho; Jahng, Jeong Won

doi:10.5607/en.2010.19.3.132

Cited by 5 publications

(4 citation statements)

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“…In control non-pregnant rats, pERK1/2 expression was found to be ~50 pERK1/2-positive cells in the SON and ~180-pERK1/2 positive cells in the PVN. These numbers are higher but comparable to previous studies, where control animals have pERK1/2-positive cells on average around 20 and 100 in the SON and PVN, respectively 299,313 . There are limited studies that documented p-p38 expression in the SON or PVN.…”

Section: Basal Perk1/2 and P-p38 Expression In Son And Pvn Neurons Of Control Nonpregnant Ratssupporting

confidence: 89%

Kisspeptin Regulation of Oxytocin Neuron Activity in Late Pregnancy

et al. 2020

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Oxytocin is secreted from the posterior pituitary gland by oxytocin neurons to trigger uterine contractions during birth. We have recently shown that the oxytocin neuron firing rate increases in response to intracerebroventricular (ICV) kisspeptin only in late‐pregnant rats. Furthermore, the kisspeptin projection from the periventricular nucleus of the hypothalamus (PeN) to the perinuclear zone (PNZ) surrounding the supraoptic nucleus (SON) increases in late pregnancy. This study aimed to determine the site and mechanism of central kisspeptin activation of oxytocin neuron activity in late pregnant rats. First, in vivo extracellular single unit recordings were made from SON neurons in urethane‐anaesthetised non‐pregnant and late‐pregnant rats during microdialysis application of kisspeptin (100 μM in the dialysate) into the SON. Intra‐SON kisspeptin consistently increased the firing rate of oxytocin neurons in late‐pregnant rats but not in non‐pregnant rats. Two‐way repeated measures (RM) ANOVA revealed a significant interaction between REPRODUCTIVE STATUS and TIME (F(6,88) = 10.31, p < 0.001); post hoc all pairwise Holm‐Sidak tests revealed a significant increase in firing rate in late‐pregnant rats at 30 (p < 0.05), 40, 50 and 60 minutes (all p < 0.001 versus pre‐kisspeptin), and a significantly higher firing rate than in time‐matched recordings from non‐pregnant rats at 50 and 60 minutes (p < 0.05). Then, to examine whether excitatory effects of central kisspeptin emerges directly within the SON and paraventricular nucleus (PVN) containing oxytocin neurons, we performed single label diaminobenzidine (DAB) immunostaining against phosphorylated extracellular regulated kinase (pERK), a second messenger activated by kisspeptin. ICV cannulae were implanted on day 13 or 14‐pregnant and non‐pregnant rats and one week later, day 21 pregnant and non‐pregnant rats were perfused 15 min after ICV administration of kisspeptin (2 μg/2 μl) or vehicle under pentobarbital anaesthesia. ICV kispeptin injection did not alter pERK expression in the SON or PVN. Two‐way RM ANOVA revealed a significant effect of REPRODUCTIVE STATUS (F(1,28) = 4.78, p = 0.03) but no significant effect of TREATMENT (kisspeptin/vehicle) (F(1,28) = 0.04, p = 0.82) and no REPRODUCTIVE STATUS X TREATMENT interaction (F(1,28) = 0.81, p = 0.37 ) in the SON. There was no significant effect of REPRODUCTIVE STATUS (F(1,27) = 0.93, p = 0.34, two‐way RM ANOVA) or TREATMENT (F(1,27) = 0.93, p = 0.34) and no REPRODUCTIVE STATUS X TREATMENT interaction (F(1,27) = 0.29, p = 0.59) in the PVN. Similarly, there was no significant effect of REPRODUCTIVE STATUS (F(1,27) = 2.28, p = 0.14, two‐way RM ANOVA) or TREATMENT (F(1,27) = 0.28, p = 0.59) and no REPRODUCTIVE STATUS X TREATMENT interaction (F(1,27) = 0.07, p = 0.78) in the magnocellular division of PVN. Hence, it appears that kisspeptin excites oxytocin neurons at the end of pregnancy by a presynaptic action at local nerve terminals to stimulate peripheral oxytocin release and so might contribute to oxytocin neuron act...

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Section: Basal Perk1/2 and P-p38 Expression In Son And Pvn Neurons Of Control Nonpregnant Ratssupporting

confidence: 89%

Kisspeptin Regulation of Oxytocin Neuron Activity in Late Pregnancy

et al. 2020

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“…[40][41][42] Active lowering of serotonin levels results in increased NPY levels, 43 while induction of 5-HT signalling showed to reduce NPY levels in rat hypothalamus. 44 More importantly, serotonin is able to repress food intake, despite weight loss-induced elevation of messenger NPY, 45 suggesting that serotonin might act as an interfering factor between transcription and NPY secretion. Therefore, we hypothesized that serotonin might interfere with NPY signalling at a post-transcriptional level.…”

Section: Discussionmentioning

confidence: 99%

Differences in food intake of tumour‐bearing cachectic mice are associated with hypothalamic serotonin signalling

Dwarkasing

Boekschoten

Argilés

et al. 2015

J cachexia sarcopenia muscle

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BackgroundAnorexia is a common symptom among cancer patients and contributes to malnutrition and strongly impinges on quality of life. Cancer-induced anorexia is thought to be caused by an inability of food intake-regulating systems in the hypothalamus to respond adequately to negative energy balance during tumour growth. Here, we show that this impaired response of food-intake control is likely to be mediated by altered serotonin signalling and by failure in post-transcriptional neuropeptide Y (NPY) regulation.MethodsTwo tumour cachectic mouse models with different food intake behaviours were used: a C26-colon adenocarcinoma model with increased food intake and a Lewis lung carcinoma model with decreased food intake. This contrast in food intake behaviour between tumour-bearing (TB) mice in response to growth of the two different tumours was used to distinguish between processes involved in cachexia and mechanisms that might be important in food intake regulation. The hypothalamus was used for transcriptomics (affymetrix chips).ResultsIn both models, hypothalamic expression of orexigenic NPY was significantly higher compared with controls, suggesting that this change does not directly reflect food intake status but might be linked to negative energy balance in cachexia. Expression of genes involved in serotonin signalling showed to be different between C26-TB mice and Lewis lung carcinoma-TB mice and was inversely associated with food intake. In vitro, using hypothalamic cell lines, serotonin repressed neuronal hypothalamic NPY secretion while not affecting messenger NPY expression, suggesting that serotonin signalling can interfere with NPY synthesis, transport, or secretion.ConclusionsAltered serotonin signalling is associated with changes in food intake behaviour in cachectic TB mice. Serotonins' inhibitory effect on food intake under cancer cachectic conditions is probably via affecting the NPY system. Therefore, serotonin regulation might be a therapeutic target to prevent the development of cancer-induced eating disorders.

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“…In addition, decreasing serotonin concentrations by inhibiting serotonin synthesis results in increased NPY levels [154]. Furthermore, these effects of serotonin on feeding and NPY levels are not apparently accomplished via affecting NPY gene expression [154,155]. Also in vitro, serotonin inhibits neuronal NPY secretion, while not affecting NPY gene expression [93].…”

Section: Serotonin As Upstream Regulator Of Hypothalamic Resistancementioning

confidence: 95%