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Hypothalamic Arcuate Nucleus (hypothalamic + arcuate_nucleus)
Selected AbstractsAltered Expression of SOCS3 in the Hypothalamic Arcuate Nucleus during Seasonal Body Mass Changes in the Field Vole, Microtus agrestisJOURNAL OF NEUROENDOCRINOLOGY, Issue 2 2007E. Król We have previously shown that cold-acclimated (8 °C) male field voles (Microtus agrestis) transferred from short day (SD, 8 h light) to long day (LD, 16 h light) photoperiod exhibit an increase in body mass lasting 4 weeks, after which they stabilise at a new plateau approximately 7.5 g (24.8%) higher than animals maintained in SD. By infusing voles with exogenous leptin, we have also demonstrated that SD voles respond to the hormone by reducing body mass and food intake, whereas LD animals increasing body mass are resistant to leptin treatment. In the present study, we investigated whether seasonal changes in body mass could be linked to modulation of the leptin signal by suppressor of cytokine signalling-3 (SOCS3). We used in situ hybridisation to examine hypothalamic arcuate nucleus (ARC) expression of SOCS3, neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) genes in 90 voles exposed to either SD or LD for up to 11 weeks. LD voles increasing body mass had significantly higher levels of SOCS3 mRNA than SD or LD voles with a stable body mass. There were no associated changes in expression of NPY, AgRP, POMC and CART genes. These results suggest that voles that regulate body mass at either the lower (SD) or upper (LD) plateau remain sensitive to leptin action, whereas SOCS3-mediated leptin resistance is a short-term mechanism that enables animals to move between the stable body mass plateaus. Our data provide evidence that expression of SOCS3 in the ARC is involved in the modulation of the strength of the leptin signal to facilitate seasonal cycles in body mass and adiposity. [source] Changes in Expression of the Genes for the Leptin Receptor and the Growth Hormone-Releasing Peptide/Ghrelin Receptor in the Hypothalamic Arcuate Nucleus with Long-Term Manipulation of Adiposity by Dietary MeansJOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2005Y. Kurose Abstract Changes in leptin and ghrelin levels occur with alterations in adiposity, but signalling may be affected by levels of the relevant receptors. We measured expression of the leptin receptor (Ob-Rb) and the ghrelin/growth hormone releasing peptide receptor (GHS-R) in the arcuate nucleus of sheep held at either high or low levels of adiposity. Plasma growth hormone (GH) levels were lower in Fat animals and higher in Lean animals. Plasma insulin and leptin levels were higher in Fat animals and lower in Lean animals. Frozen hypothalamic sections of arcuate nucleus were extracted and mRNA levels measured for mRNA for Ob-Rb and GHS-R. Gene expression for both Ob-Rb and GHS-R was higher in Lean animals than in Fat animals, with no difference in expression between Fat and Normal animals. A second group of animals (n = 4 per group) was used for double-labelling immunohistochemistry to determine whether the increase in Ob-Rb gene expression was translated into Ob-Rb protein and to ascertain whether this effect is localised to the cells of the arcuate nucleus that produce either neuropeptide Y (NPY) and/or pro-opiomelanocortin-derived peptides. Lean animals displayed a 255% increase in immunoreactive NPY cells (P < 0.005), a 167% increase in cells with Ob-Rb (P < 0.037) protein and a 344% increase in cells that were staining for both NPY and Ob-Rb (P < 0.02). There was no difference between the Normal and Lean animals in the number of cells that were detected with an adrenocorticotrophic hormone (ACTH) antibody or the number of ACTH-immunoreactive cells that also stained for Ob-Rb. Finally, we measured plasma ghrelin levels in Normal, Fat and Lean ewes (n = 4/group); levels were higher (P < 0.05) in Fat animals than in Lean animals. We conclude that lowering body weight leads to increased expression of Ob-Rb, ghrelin/GHS-R expression and proportion of NPY cells that express Ob-Rb in the arcuate nucleus. This may be an adaptive mechanism to increase responsivity to both leptin and ghrelin. [source] Systemic Administration of Ghrelin Induces Fos and Egr-1 Proteins in the Hypothalamic Arcuate Nucleus of Fasted and Fed RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 11 2000A. K. Hewson Abstract Ghrelin, a recently identified endogenous ligand for the growth hormone secretagogue (GHS) receptor, induces growth hormone (GH) secretion following systemic administration. We sought to determine whether systemic administration of ghrelin activates cells in the hypothalamic arcuate nucleus by examining the distribution of cells expressing Fos and Egr-1 proteins. In normally fed rats, both ghrelin and GHRP-6 (a synthetic GHS) significantly increased the number of cells expressing Fos and Egr-1 in the arcuate nucleus. The effects of ghrelin and GHRP-6 to induce Fos or Egr-1 protein expression was significantly greater in fasted than in fed rats. Thus, we show that (i) ghrelin is a centrally active peptide; (ii) it acts in a similar manner to synthetic GHS; and (iii) its central actions are increased in fasting, presumably reflecting physiological changes that accompany altered food intake and/or nutritional state. [source] Physiological functions of glucose-inhibited neuronesACTA PHYSIOLOGICA, Issue 1 2009D. Burdakov Abstract Glucose-inhibited neurones are an integral part of neurocircuits regulating cognitive arousal, body weight and vital adaptive behaviours. Their firing is directly suppressed by extracellular glucose through poorly understood signalling cascades culminating in opening of post-synaptic K+ or possibly Cl, channels. In mammalian brains, two groups of glucose-inhibited neurones are best understood at present: neurones of the hypothalamic arcuate nucleus (ARC) that express peptide transmitters NPY and agouti-related peptide (AgRP) and neurones of the lateral hypothalamus (LH) that express peptide transmitters orexins/hypocretins. The activity of ARC NPY/AgRP neurones promotes food intake and suppresses energy expenditure, and their destruction causes a severe reduction in food intake and body weight. The physiological actions of ARC NPY/AgRP cells are mediated by projections to numerous hypothalamic areas, as well as extrahypothalamic sites such as the thalamus and ventral tegmental area. Orexin/hypocretin neurones of the LH are critical for normal wakefulness, energy expenditure and reward-seeking, and their destruction causes narcolepsy. Orexin actions are mediated by highly widespread central projections to virtually all brain areas except the cerebellum, including monosynaptic innervation of the cerebral cortex and autonomic pre-ganglionic neurones. There, orexins act on two specific G-protein-coupled receptors generally linked to neuronal excitation. In addition to sensing physiological changes in sugar levels, the firing of both NPY/AgRP and orexin neurones is inhibited by the ,satiety' hormone leptin and stimulated by the ,hunger' hormone ghrelin. Glucose-inhibited neurones are thus well placed to coordinate diverse brain states and behaviours based on energy levels. [source] Hormonal enhancement of neuronal firing is linked to structural remodelling of excitatory and inhibitory synapsesEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2002A. Parducz Abstract The ovarian hormone estradiol induces morphological changes in the number of synaptic inputs in specific neuronal populations. However, the functional significance of these changes is still unclear. In this study, the effect of estradiol on the number of anatomically identified synaptic inputs has been assessed in the hypothalamic arcuate nucleus. The number of axo-somatic, axodendritic and spine synapses was evaluted using unbiased stereological methods and a parallel electrophysiological study was performed to assess whether synaptic anatomical remodelling has a functional consequence on the activity of the affected neurons. Estradiol administration to ovariectomized rats induced a decrease in the number of inhibitory synaptic inputs, an increase in the number of excitatory synapses and an enhancement of the frequency of neuronal firing. These results indicate that oestrogen modifications in firing frequency in arcuate neurons are temporally linked to anatomical modifications in the numerical balance of inhibitory and excitatory synaptic inputs. [source] Postnatal glutamate-induced central nervous system lesions alter periodontal disease susceptibility in adult Wistar ratsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 10 2001Torbjørn Breivik Abstract Background: Inability to mount a suitable brain-neuroendocrine response to bacterial or other antigenic challenges has been found to play an important rôle in infectious and inflammatory disease susceptibility and progression, including periodontal disease. Objective: The present study was designed to determine the effects of glutamate administration to new-born Wistar rats on the development and progression of naturally occurring and ligature-induced periodontal disease in the rats as adults. Postnatal glutamate administration is known to permanently damage neurones in the hypothalamic arcuate nucleus. Method: New-born rats were treated 1× daily subcutaniously with 2 mg/g of monosodium-L-glutamate (MSG) for 5 days from day 3 to 6. Control animals were injected with similar amounts of saline. Experimental ligature-induced periodontal disease was induced in the rats at the age of 12 weeks at maxillary right 2nd molar teeth. The contralateral maxillary left 2nd molars served as control teeth, and for assessment of naturally occurring periodontal disease. Disease progression was evaluated histometrically. Results: The results revealed that the glutamate-lesioned rats developed significantly more periodontal tissue destruction compared to sham-lesioned control rats in both the ligated and non-ligated teeth. Conclusions: This study supports our resent findings indicating that inappropriate brain-neuroendocrine-immune regulation may play a rôle in periodontal disease susceptibility and progression. Zusammenfassung Hintergrund: Es hatte gezeigt werden können, dass die Unfähigkeit des Gehirns auf einen bakteriellen oder antigenen Reiz mit einer angemessenen neuroendokrinen Antwort zu reagieren, eine wichtige Rolle für die Empfänglichkeit für infektiöse und entzündliche Erkrankungen einschliesslich Parodontitis spielt. Die Gabe von Glutamat nach der Geburt führt zu irreversiblen Schäden der Neurone des Nucleus arcuatus des Hypothalamus. Zielzetzung: Untersuchung der Auswirkungen von Glutamatgaben bei neugeborenen Wistar-Ratten auf die Entstehung und das Fortschreiten natürlich vorkommender und ligaturinduzierter Parodontitis im Erwachsenenalter. Material und Methoden: Bei 24 neugeborenen Wistar-Ratten wurden einmal täglich 2 mg/g L-Mononatriumglutamat und bei 20 Kontrolltieren statt dessen Kochsaltzlösung vom 4. Lebenstag an 4 Tage lang subkutan injiziert. Am rechten zweiten Oberkiefermolaren wurden bei den 12 Wochen alten Ratten eine experimentelle ligaturinduzierte Parodontitis ausgelöst. Der kontralaterale 2. Molar des Oberkiefers diente als Kontrolle und um natürlich vorkommende Parodontitis zu untersuchen. Das Fortschreiten der parodontalen Zerstörung wurde histometrisch erfasst. Ergebnisse: Die Ergebnisse zeigten, dass die Ratten mit den glutamatinduzierten Läsionen statistisch signifikant stärkere parodontale Zerstörungen sowohl an den Zähnen mit wie auch an denen ohne Ligaturen im Vergleich zur Kontrollgruppe aufwiesen. Schlussfolgerungen: Eine unangemessene neuroendokrinoimmunologische Regulation des Gehirns scheint eine Rolle bei der Empfänglichkeit für und das Fortschreiten von Parodontitis zu haben. Résumé Origine: L'incapacitéàétablir une réponse neuroendocrinienne cervicale efficace pour des défis bactériens ou antigèniques joue un rôle important dans la susceptibilité et la progression des maladies infectieuses et inflammatoires, dont les parodontites. But: Cette étude a été imaginée pour déterminer les effets de l'administration de glutamate à des rats Wistar nouveau-nés sur le développement et la progression de maladies parodontales naturelles et induites par des ligatures chez le rat adulte. On sait que l'administration de glutamate en postnatal endommage de façon permanente les neurones du noyau d'arc hypothalamique. Méthodes: Les rats nouveaus-nés furent traités une fois par jour par administration sous cutanée de 2 mg/g de monosodium-L-glutamate (MSG) pendant 5 jours. Les animaux contrôles recevaient une dose similaire de sérum physiologique. La parodontite expérimentale par ligature était réalisée à l'âge de 12 semaines, sur la deuxième molaire supérieure droite. La dent controlatérale servait de contrôle et à la mise en évidence de maladie parodontale naturelle. La progression de la maladie fut évaluée par histométrie. Résultats: Les résultats montrent que les rats atteints de lésions dues au glutamate développent plus de destructions parodontales (par ligatures ou sans ligatures) par rapport aux rats contrôles atteints de lésions simulées. Conclusion: Cette étude supporte nos récentes découvertes qui indiquent qu'une régulation immunitaire neuroendocrinienne cervicale inappropriée peut jouer un rôle dans la susceptibilité et la progression des maladies parodontales. [source] Possible Role of Oestrogen in Pubertal Increase of Kiss1/Kisspeptin Expression in Discrete Hypothalamic Areas of Female RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2009K. Takase Kisspeptin, a peptide encoded by the Kiss1 gene, has been considered as a potential candidate for a factor triggering the onset of puberty, and its expression in the hypothalamus was found to increase during peripubertal period in rodent models. The present study aimed to clarify the oestrogenic regulation of peripubertal changes in Kiss1 mRNA expression in the anteroventral periventricular nucleus (AVPV) and hypothalamic arcuate nucleus (ARC), and to determine which population of kisspeptin neurones shows a change in kisspeptin expression parallel to that in luteinising hormone (LH) pulses at the peripubertal period. Quantitative reverse transcriptase-polymerase chain reaction and immunohistochemistry revealed an apparent increase in the ARC Kiss1 mRNA expression and kisspeptin immunoreactivity around the time of vaginal opening in intact female rats. The AVPV Kiss1 mRNA levels also increased at day 26, but decreased at day 31, and then increased at day 36/41. In ovariectomised (OVX) rats, ARC Kiss1 mRNA expression did not show peripubertal changes and was kept at a high level throughout peripubertal periods. Apparent LH pulses were found in these prepubertal OVX rats. Oestradiol replacement suppressed ARC Kiss1 mRNA expression in OVX prepubertal rats, but not in adults. Similarly, LH pulses were suppressed by oestradiol in the prepubertal period (days 21 and 26), but regular pulses were found in adulthood. The present study suggests that a pubertal increase of Kiss1/kisspeptin expression both in the ARC and AVPV is involved in the onset of puberty. These results also suggest that both LH pulses and ARC Kiss1 expression are more negatively regulated by oestrogen in prepubertal female rats compared to adult rats. [source] Altered Expression of SOCS3 in the Hypothalamic Arcuate Nucleus during Seasonal Body Mass Changes in the Field Vole, Microtus agrestisJOURNAL OF NEUROENDOCRINOLOGY, Issue 2 2007E. Król We have previously shown that cold-acclimated (8 °C) male field voles (Microtus agrestis) transferred from short day (SD, 8 h light) to long day (LD, 16 h light) photoperiod exhibit an increase in body mass lasting 4 weeks, after which they stabilise at a new plateau approximately 7.5 g (24.8%) higher than animals maintained in SD. By infusing voles with exogenous leptin, we have also demonstrated that SD voles respond to the hormone by reducing body mass and food intake, whereas LD animals increasing body mass are resistant to leptin treatment. In the present study, we investigated whether seasonal changes in body mass could be linked to modulation of the leptin signal by suppressor of cytokine signalling-3 (SOCS3). We used in situ hybridisation to examine hypothalamic arcuate nucleus (ARC) expression of SOCS3, neuropeptide Y (NPY), agouti-related peptide (AgRP), pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) genes in 90 voles exposed to either SD or LD for up to 11 weeks. LD voles increasing body mass had significantly higher levels of SOCS3 mRNA than SD or LD voles with a stable body mass. There were no associated changes in expression of NPY, AgRP, POMC and CART genes. These results suggest that voles that regulate body mass at either the lower (SD) or upper (LD) plateau remain sensitive to leptin action, whereas SOCS3-mediated leptin resistance is a short-term mechanism that enables animals to move between the stable body mass plateaus. Our data provide evidence that expression of SOCS3 in the ARC is involved in the modulation of the strength of the leptin signal to facilitate seasonal cycles in body mass and adiposity. [source] Systemic Administration of Ghrelin Induces Fos and Egr-1 Proteins in the Hypothalamic Arcuate Nucleus of Fasted and Fed RatsJOURNAL OF NEUROENDOCRINOLOGY, Issue 11 2000A. K. Hewson Abstract Ghrelin, a recently identified endogenous ligand for the growth hormone secretagogue (GHS) receptor, induces growth hormone (GH) secretion following systemic administration. We sought to determine whether systemic administration of ghrelin activates cells in the hypothalamic arcuate nucleus by examining the distribution of cells expressing Fos and Egr-1 proteins. In normally fed rats, both ghrelin and GHRP-6 (a synthetic GHS) significantly increased the number of cells expressing Fos and Egr-1 in the arcuate nucleus. The effects of ghrelin and GHRP-6 to induce Fos or Egr-1 protein expression was significantly greater in fasted than in fed rats. Thus, we show that (i) ghrelin is a centrally active peptide; (ii) it acts in a similar manner to synthetic GHS; and (iii) its central actions are increased in fasting, presumably reflecting physiological changes that accompany altered food intake and/or nutritional state. [source] Brain Catalase Inhibition Blocks Ethanol-Related Decrease of Blood Luteinizing Hormone Levels in MiceALCOHOLISM, Issue 8 2002Carles Sanchis-Segura Background It has been demonstrated that ethanol decreases blood luteinizing hormone (LH) levels in rodents. This effect seems to be produced by the capacity of ethanol to release ,-endorphins from the hypothalamic arcuate nucleus and, in a second step, by a ,-receptor,mediated inhibitory effect of these peptides on hypothalamic LH-releasing hormone-synthesizing neurons. However, it has been reported that, in primary hypothalamic cultures, the ethanol-produced ,-endorphin release is mediated by the enzyme catalase. Therefore, the aim of this study was to assess whether catalase inhibition modifies ethanol effects on blood LH levels. Methods Swiss albino mice were pretreated with the catalase inhibitor 3-amino-1,2,4-triazole (AT; 0.0,0.5 g/kg) and, 3.5 hr later, saline, ethanol (2.5 g/kg), or morphine (30 mg/kg) was administered. Blood samples were collected 2 hr after ethanol administration, and LH levels were immunoenzymatically assayed. Results The catalase inhibitor AT dose-dependently blocked the ethanol-produced decrease in blood LH levels without altering those observed after saline or morphine administration. This effect was highly correlated with the decrease in brain catalase activity produced by AT. Conclusions These results show an antagonistic effect between AT and ethanol on blood LH levels and suggest a role of brain catalase activity on this effect of ethanol. Data are discussed in terms of a possible functional relationship between brain catalase and ,-endorphins in the mediation of some of the psychopharmacological consequences observed after ethanol administration. [source] Gene expression in arcuate nucleus-median eminence of rats treated with leptin or ciliary neurotrophic factorBIOFACTORS, Issue 2 2007Suresh Ambati Abstract Ciliary neurotrophic factor (CNTF) and leptin are cytokine-like hormones and act on their corresponding receptors in the hypothalamic arcuate nucleus (ARC). The present study was designed to assess effects of intracerebroventricular (ICV) injection of leptin and CNTF on gene expression in micropunched hypothalamic arcuate nucleus-median eminence (ARCME) complex samples from rats. Male Sprague Dawley rats were implanted with lateral cerebroventricular cannulas for administration of control, 10 ,g/d leptin or 5 ,g/d CNTF for four days. Real-time Taqman RT-PCR was used to quantitatively compare the mRNA levels of selected genes in the ARC-ME complex. Leptin and CNTF increased ARC-ME mRNA levels of signal transducer and activator of transcription 3 (STAT3) by 64.5 and 124.7% (p < 0.01), suppressor of cytokine signaling 3 (SOCS3) by 258.9 and 1063.9% (p < 0.01), cocaine and amphetamine regulated transcript (CART) by 102.7 and 123.1% (p < 0.01), and proopiomelanocortin (POMC2) by 374.1 and 264.9% (p < 0.01), respectively. Leptin increased growth hormone releasing hormone (GHRH) by 309.9% (p < 0.01), while CNTF increased janus kinase 2 (JAK2) mRNA by 31.7% (p < 0.01) and decreased gonadotropin releasing hormone 1 (GNRH1) by 59.7% (p < 0.01), mitogen activated protein kinase 1 (MAPK1) by 19.4% (p < 0.05) and tyrosine hydroxylase (TH) by 74.5% (p < 0.05). Significant reduction in daily food intake and body weights by both the treatments was observed. Also, decrease in weights of fat pads was concomitant with lowered serum insulin and leptin levels. Our findings show that leptin and CNTF engage both convergent and divergent pathways involved in feeding, cellular signaling, inflammation, and other related regulatory systems. [source] | |||||||||||||