Distribution of estrogen receptor-beta messenger ribonucleic acid in the male sheep hypothalamus.
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As a first step in determining possible influences of the newly discovered estrogen receptor (ER)-beta on reproduction, we have localized mRNA for ER-beta within the male sheep hypothalamus using in situ hybridization and a rat ER-beta cRNA probe. Highest amounts of hybridization signal were observed in the preoptic area (POA), bed nucleus of the stria terminalis, paraventricular nucleus, and supraoptic nucleus. Relatively moderate amounts of hybridization signal were observed in the retrochiasmatic area (RCH), anterior hypothalamic area, dorsomedial hypothalamus, and lateral hypothalamus. Only a low level of hybridization signal was observed in the ventromedial hypothalamus, suprachiasmatic nucleus, and arcuate nucleus. The presence of ER-beta mRNA in several areas of the male sheep hypothalamus suggests multiple functions for this receptor. The distribution of ER-beta in the ovine hypothalamus was similar to that described for the rat, suggesting a high degree of functional conservation across species. A role for ER-beta in influencing reproduction is suggested by its presence in the POA and RCH, regions of the hypothalamus that control reproduction. (+info)
D1 and D2 dopamine receptor messenger ribonucleic acid in brain and pituitary during the reproductive cycle of the turkey hen.
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The regulation of prolactin secretion during the reproductive cycle of seasonal breeding birds appears to be largely under the stimulatory influence of hypothalamic vasoactive intestinal peptide (VIP). However, the factors influencing VIP secretion, and hence prolactin release, in birds remain largely unexplored. Recent evidence has demonstrated that dopamine and dopamine receptors may affect VIP and prolactin release in birds. The differential expression of dopamine receptors on hypothalamic VIP-releasing neurons may affect the degree of prolactinemia observed during the reproductive cycle of birds. In order to examine this hypothesis, we used reverse transcription-polymerase chain reaction to quantitate the levels of D1 and D2 dopamine receptor subtype mRNAs in the brain of the domestic turkey hen during the reproductive cycle. No significant difference in hypothalamic expression of D1 or D2 dopamine receptor subtypes during the reproductive cycle was observed. However, pronounced differences in D1D and D2 mRNAs were detected in cortex and cerebellum. Interestingly, there was a dramatic increase in pituitary D1D receptor mRNA during the reproductive stages of laying and incubation of eggs, which paralleled the hyperprolactinemic state of the turkey reproductive cycle. In addition, pituitary D2 receptor mRNA steadily increased throughout the reproductive cycle. In light of these observations, a modified hypothesis regarding the effects of dopamine on prolactin secretion is discussed. (+info)
An autoradiographic analysis of [3H]alpha-bungarotoxin distribution in the rat brain after intraventricular injection.
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Purified alpha-bungarotoxin was isolated by chromatography and made radioactive with tritium ([3H]acetamidino-alpha-bungarotoxin). Infusions of [3H]alpha-bungarotoxin alone or preceded by tubocurarine or atropine were given into the third ventricle. 2. 12, or 24 h after injection the brains were prepared for autoradiography. Injections of alpha-bungarotoxin (radioinert) in buffer, or of [3H]parathyroid hormone in buffer, served as controls. The various patterns of labeling suggest the presence of nicotinic-cholinergic neurons within the arcuate and basolateral regions of the hypothalamus including the supraoptic and suprachiasmatic nuclei and, in addition, the central nucleus of the amygdala. (+info)
Properties of C1 and other ventrolateral medullary neurones with hypothalamic projections in the rat.
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1. This study compared (i) the properties of C1 cells with those of neighbouring non-C1 neurones that project to the hypothalamus and (ii) the properties of C1 cells that project to the hypothalamus with those of their medullospinal counterparts. 2. Extracellular recordings were made at three rostrocaudal levels of the ventrolateral medulla (VLM) in alpha-chloralose-anaesthetized, artificially ventilated, paralysed rats. Recorded cells were filled with biotinamide. 3. Level I (0-300 microm behind facial nucleus) contained spontaneously active neurones that were silenced by baro- and cardiopulmonary receptor activation and virtually unaffected by nociceptive stimulation (firing rate altered by < 20 %). These projected either to the cord (type I; 36/39), or to the hypothalamus (type II; 2/39) but rarely to both (1/39). 4. Level II (600-800 microm behind facial nucleus) contained (i) type I neurones (n = 3) (ii) type II neurones (n = 11), (iii) neurones that projected to the hypothalamus and were silenced by baro- and cardiopulmonary receptor activation but activated by strong nociceptive stimulation (type III, n = 2), (iv) non-barosensitive cells activated by weak nociceptive stimulation which projected only to the hypothalamus (type IV, n = 9), (v) cells that projected to the hypothalamus and responded to none of the applied stimuli (type V, n = 7) and (vi) neurones activated by elevating blood pressure which projected neither to the cord nor to the hypothalamus (type VI, n = 4). 5. Level III (1400-1600 microm behind facial motor nucleus) contained all the cell types found at level II except type I. 6. Most of type I and II (17/26) and half of type III cells (4/8) were C1 neurones. Type IV-V were rarely adrenergic (2/12) and type VI were never adrenergic (0/3). 7. All VLM baroinhibited cells project either to the cord or the hypothalamus and virtually all (21/23) C1 cells receive inhibitory inputs from arterial and cardiopulmonary receptors. (+info)
Altered energy balance causes selective changes in melanocortin-4(MC4-R), but not melanocortin-3 (MC3-R), receptors in specific hypothalamic regions: further evidence that activation of MC4-R is a physiological inhibitor of feeding.
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We have examined the effects of underfeeding and obesity on the density of hypothalamic melanocortin MC3 and MC4 receptors (MC3-R and MC4-R, respectively), which may mediate the hypophagic effects of alpha-melanocyte-stimulating hormone (MSH) in the rat. MC3-R and MC4-R were measured by quantitative autoradiography in brain sections using 125I-labeled Nle4-D-Phe7-alpha-MSH (125I-NDP-MSH) and discriminated by masking MC3-R with excess unlabelled gamma2-MSH. High densities of MC4-R occurred in the ventromedial (VMH) and arcuate (ARC) nuclei, median eminence (ME), and medial habenular nucleus (MHb), with lower densities in the dorsomedial hypothalamus (DMH) and forebrain regions. MC3-R were confined to the VMH, ARC, and MHb. After 10-days of food restriction (14% weight loss), density of MC4-R was significantly increased by 20-65% in the VMH, ARC, ME, and DMH, with no changes elsewhere. Similarly, obese (fa/fa) Zucker rats showed 43-98% increases in MC4-R in the same regions. By contrast, rats with diet-induced obesity (18% heavier than controls) showed significantly decreased binding to MC4-R, especially in the VMH, ARC, and ME. MC3-R showed no significant alterations in any model. We suggest that increased density of MC4-R with food restriction and in obese Zucker rats reflects receptor upregulation secondary to decreased release of alpha-MSH, consistent with increased hunger in these models. Conversely, downregulation of MC4-R in diet-induced obesity may indicate increased alpha-MSH secretion in an attempt to limit overeating. This alpha-MSH/MC4-R system may be inhibited by leptin and/or insulin. MC3-R are not apparently involved in regulating feeding. (+info)
Induction of obesity and hyperleptinemia by central glucocorticoid infusion in the rat.
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It has been claimed that factors favoring the development or maintenance of animal or human obesity may include increases in glucocorticoid production or hyperresponsiveness of the hypothalamic-pituitary-adrenal axis. In normal rats, glucocorticoids have been shown to be necessary for chronic intracerebroventricular infusion of neuropeptide Y to produce obesity and related abnormalities. Conversely, glucocorticoids inhibited the body weight-lowering effect of leptin. Such dual action of glucocorticoids may occur within the central nervous system, since both neuropeptide Y and leptin act within the hypothalamus. The aim of this study was to determine the effects of glucocorticoids (dexamethasone) given intracerebroventricularly to normal rats on body weight homeostasis and hypothalamic levels of neuropeptide Y and corticotropin-releasing hormone. Continuous central glucocorticoid infusion for 3 days resulted in marked sustained increases in food intake and body weight relative to saline-infused controls. The infusion abolished endogenous corticosterone output and produced hyperinsulinemia, hypertriglyceridemia, and hyperleptinemia, three salient abnormalities of obesity syndromes. Central glucocorticoid infusion also produced a marked decrease in the expression of uncoupling protein (UCP)-1 and UCP-3 in brown adipose tissue and UCP-3 in muscle. Finally, chronic central glucocorticoid administration increased the hypothalamic levels of neuropeptide Y and decreased those of corticotropin-releasing hormone. When the same dose of glucocorticoids was administered peripherally, it resulted in decreases in food intake and body weight, in keeping with the decrease in hypothalamic neuropeptide Y levels. These results suggest that glucocorticoids induce an obesity syndrome in rodents by acting centrally and not peripherally. (+info)
T-lymphocyte activation increases hypothalamic and amygdaloid expression of CRH mRNA and emotional reactivity to novelty.
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Stimulation of T-cells with staphylococcal enterotoxin B (SEB) significantly elevates interleukin-2 (IL-2) and contemporaneous activation of the hypothalamic-pituitary-adrenal (HPA) axis and c-fos in the paraventricular nucleus (PVN) of BALB/cByJ mice. Such neural signaling may promote cognitive and emotional adaptation before or during infectious illness. Because corticotropin-releasing hormone (CRH) is an anxiogenic neuropeptide that may mediate the stressor-like effects of immunological stimuli, we measured neuronal CRH mRNA alterations in mice challenged with SEB. Increased CRH mRNA levels were observed in the PVN and central nucleus of the amygdala (ceA) 4-6 hr after SEB administration. This was associated with plasma ACTH increases, which could be abrogated by the systemic administration of anti-CRH antiserum. Additional experiments did not support a role for IL-2 or prostaglandin synthesis in activating the HPA axis. Behavioral experiments testing for conditioned taste aversion did not confirm that SEB challenge promotes malaise. However, consistent with the notion that central CRH alterations induced by SEB may affect emotionality (e.g., fear), SEB challenge augmented appetitive neophobia in a context-dependent manner, being marked in a novel and stressful environment. It is hypothesized that immunological stimuli generate a cascade of events that solicit integrative neural processes involved in emotional behavior. As such, these data support the contention that affective illness may be influenced by immunological processes and the production of cytokines and are consistent with other evidence demonstrating that autoimmune reactivity is associated with enhanced emotionality. (+info)
Expression of the vasotocin gene in the hypothalamus of intact and osmotically stimulated bullfrogs during metamorphosis.
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To study the ontogeny of the vasotocin (VT) system and its contribution to anuran metamorphosis, VT mRNA levels were determined by Northern blot analysis in metamorphosing bullfrog tadpoles. Effects of osmotic stimulation on VT mRNA levels were also analyzed in order to follow the development of osmotic responsiveness of VT neurons. The intensity of hybridization signals for VT mRNA gradually increased during prometamorphic development. The increase became marked thereafter until metamorphic climax. Plasma osmolality and hematocrit remained unchanged before metamorphosis, and increased after metamorphic climax, indicating that climactic tadpoles in a semi-terrestrial environment were in a dehydrated condition. These increases correlated well with the increase in VT mRNA level. Immersion of tadpoles in 30% seawater (approximately 350 mOsmol) for 3 days increased plasma osmolality at all stages. No significant changes were observed in the VT mRNA level in response to this treatment during premetamorphic stages. The VT mRNA levels were significantly higher in the treated tadpoles after preclimax stages. Hyperosmotic treatment also increased hematocrit until early metamorphic climax, but did not alter it in tadpoles at late metamorphic climax. These results suggest that the responsiveness of VT-producing neurons to hyperosmotic or hypovolemic stimulation, or both, is established by the time of the metamorphic climax in bullfrog. The marked increase in VT mRNA levels at metamorphic climax stages of intact individuals is probably induced by dehydration. VT-stimulated water absorption and reabsorption in the target organs probably prevented the increase in hematocrit at late metamorphic climax. Thus VT may contribute importantly to osmoregulatory mechanisms in relation to adaptation to a semi-terrestrial habitat through the metamorphosis. (+info)