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At least 631 records · Page 35Linked to original sources
PubMed2001

The differential effect of angiotensin II and angiotensin 1-7 on norepinephrine, epinephrine, and dopamine concentrations in rat hypothalamus: the involvement of angiotensin receptors.

Angiotensin 1-7 has been recently claimed the active member of the angiotensins' family. In the present study we compared the effect of angiotensin II and angiotensin 1-7 on the concentration of dopamine, serotonin, epinephrine, and norepinephrine and some of their metabolites in the rat hypothalamus, where the levels of angiotensins are particularly high. Intracerebroventricular injection of angiotensin II, but not angiotensin 1-7, time-dependently elevated the levels of both epinephrine (p < 0.05) and norepinephrine (p < 0.05) in the hypothalamus and both effects could be prevented by intracerebroventricular injection of either AT(1) (candesartan), AT(2) (PD123319) or AT(1-7) (A-779) receptor antagonist. Neither angiotensin II nor angiotensin 1-7 produced any changes in the level of dopamine, dihydroxyphenylacetic acid, homovanilic acid, serotonin, 5-hydroxyindoleacetic acid, or tryptophan at any time point in comparison with the control groups. However, AT(1) but not AT(2) receptor blockade, unmasked the stimulatory effect of angiotensin 1-7 on dopamine concentration in the hypothalamus. Thus, angiotensin II and its active metabolite angiotensin 1-7 regulate selectively, albeit differentially, adrenergic, noradrenergic and dopaminergic systems in the hypothalamus, the effects that involve AT(1), AT(2) and AT(1-7) angiotensin receptors.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Mapping of cocaine and amphetamine regulated transcript (CART) mRNA expression in the hypothalamus of elderly human.

The expression of cocaine and amphetamine regulated transcript (CART) in the hypothalamus of aged humans was studied by in situ hybridization histochemistry. Formalin fixed coronal sections through the hypothalamus were hybridized with [35S]dATP 3' end-labeled deoxyoligonucleotide probes complementary to sequences of the CART encoding gene. Large populations of cells expressing CART messenger RNA were mainly detected in the paraventricular nucleus of the hypothalamus. Other hypothalamic subdivisions displaying numerous radiolabeled cells were the dorsomedial, ventromedial, infundibular and tuberomammillary nuclei, and the dorsal hypothalamic area. Additionally, a few labeled cells were observed in the perifornical and lateral hypothalamic areas. Hybridizing cells were occasionally seen in the supraoptic nucleus. Overall, the pattern of distribution of CART expressing cells observed throughout the human hypothalamus, with few exception, e.g. the supraoptic nucleus, is comparable to that previously reported in the rat brain. These anatomical results suggest that in human, hypothalamic CART expression could be involved a variety of neuroendocrine functions including food-intake.

Aged↗
PubMed2002

The hypothalamus in episodic brain disorders.

Episodic brain disorders (EBD) form an intriguing group of neurological diseases in which at least some of the symptoms occur in attacks. The hypothalamus integrates many brain functions, including endocrine and autonomic control, and governs various body rhythms. It seems a likely site in which the initiation of attacks of EBD can be modulated. Indeed, the hypothalamus has a crucial role in EBD such as narcolepsy and cluster headache. The same may be true for migraine and depression. Here we summarise the evidence supporting an important role for the hypothalamus in the initiation of disease episodes in various EBD. Study of the various pathophysiological concepts of EBD within the context of the hypothalamus may prove a fruitful example of cross-fertilisation between various research areas.

Animals↗
PubMed1985

Role of the anterior hypothalamus-preoptic area in the regulation of courtship behavior in the male Canadian red-sided garter snake (Thamnophis sirtalis parietalis): lesion experiments.

Lesions of the medial preoptic area and/or the ventromedial hypothalamus resulted in an abrupt and immediate decline in courtship behavior in adult male Canadian red-sided garter snakes (Thamnophis sirtalis parietalis). Lesions of the more anterior portions of the preoptic area resulted in a more gradual, delayed decline in courtship behavior. Male snakes sustaining lesions dorsal, ventral, or caudal to the anterior hypothalamus-preoptic area exhibited no change in courtship behavior relative to controls. Measurements of testis size, spermatogenic stage, and circulation levels of androgens revealed no differences between any of the groups. There were marked differences in the change in hematocrit over time between the groups. These results indicate that the anterior hypothalamus-preoptic area is involved in the control of courtship behavior in the adult male red-sided garter snake. Moreover, it is suggested that the stimulus affecting the anterior hypothalamus-preoptic area to activate courtship is temperature related.

Androgens↗
PubMed2006

Amygdala size and hypothalamus size predict social play frequency in nonhuman primates: a comparative analysis using independent contrasts.

The amygdala and hypothalamus become sexually differentiated by gonadal hormones giving rise to sexually differentiated behaviors, which include play behavior. Phylogenetic comparative analyses test for relationships between social play and brain structure volumes. Relative volume of the amygdala and hypothalamus correlated with social play, but not nonsocial play, even after controlling for the size of other brain structures. The authors propose that behaviors such as social assessment, recognizing and responding to facial expression, and social response appropriateness, which are mediated by the amygdala, are developed through social play. Additionally, the hypothalamus may regulate the motivation to engage in play through positive reinforcement of pleasurable activity. Thus, the instinctive socio-emotive aspects of play in primates appear to be those regulated by the amygdala and hypothalamus.

Amygdala↗
PubMed1984

Metabolism of exogenous noradrenaline in slices of hypothalamus and caudate nucleus of the brush-tail possum, Trichosurus vulpecula.

In the possum, Trichosurus vulpecula, the major catecholamines in the hypothalamus and caudate nucleus are noradrenaline and dopamine, respectively, suggesting that catecholaminergic transmission in these regions is similar to that in eutherian mammalian brain. Comparisons of accumulation and metabolism of 3H noradrenaline by tissue slices of the two regions indicated that in the caudate nucleus there was a seven-fold greater accumulation of unchanged noradrenaline but a lower rate of deamination to the principal metabolite, dihydroxyphenylethylene glycol (DOPEG). Cocaine inhibited DOPEG formation in the hypothalamus but not in the caudate nucleus. To explain these results, it is suggested that in the hypothalamus noradrenaline is taken up by noradrenergic nerve terminals where it undergoes extensive deamination. However, in the caudate nucleus it is taken up by, but not deaminated within, the dopaminergic nerve terminals. In the hypothalamus the presence of a corticosteroid-sensitive O-methylating system extraneuronal to noradrenergic neurones was indicated by the inhibitory effect of hydrocortisone on the O-methylation of isoprenaline. The results do not point to any major differences between the metabolism of noradrenaline in metatherian (marsupial) and eutherian brain.

Animals↗
PubMed2006

[123I]-beta-CIT SPECT imaging shows reduced thalamus-hypothalamus serotonin transporter availability in 24 drug-free obsessive-compulsive checkers.

Numerous findings indicate alterations in brain serotonin systems in obsessive-compulsive disorder (OCD). We investigated the in vivo availability of thalamus-hypothalamus serotonin transporters (SERT) in patients with DSM-IV OCD who displayed prominent behavioral checking compulsions (OC-checkers). Four hours after injection of [(123)I]-2beta-carbomethoxy-3beta-(4-iodophenyl)tropane ([(123)I]-beta-CIT), single photon emission computed tomography (SPECT) scans were performed in 24 medication-free non-depressed OC-checkers and 24 age- and gender-matched healthy controls. For quantification of brain serotonin transporter availability, a ratio of specific to non-displaceable [(123)I]-beta-CIT brain binding was used (V''(3)=(thalamus and hypothalamus-cerebellum)/cerebellum). Drug-free non-depressed OC-checkers showed an 18% reduced brain serotonin transporter availability in the thalamus and hypothalamus, as compared with healthy control subjects (1.38+/-0.19 vs 1.69+/-0.21; p<0.001). There was a strong negative correlation between severity of OC symptomatology (Y-BOCS scores) and SERT availability (r=-0.80; p<0.001). Moreover, we found a significant positive correlation between illness duration and serotonin transporter availability (r=0.43; p<0.05). This first report of significantly reduced [(123)I]-beta-CIT binding in the thalamus-hypothalamus region in OC-checkers suggests reduced brain serotonin transporter availability, which is more pronounced with increased severity of OC symptomatology and short duration of illness. The results provide direct evidence for an involvement of the serotonergic system in the pathophysiology of OCD.

Adult↗
PubMed1996

Estradiol regulation of alpha 1b-adrenoceptor mRNA in female rat hypothalamus-preoptic area.

Estradiol treatment for 48 h increases the density of alpha 1B-adrenoceptors in the hypothalamus-preoptic area of ovariectomized female rats by five- to six-fold. Present studies tested the hypothesis that estradiol elevation of hypothalamus-preoptic area alpha 1B-adrenoceptor density is correlated with increased levels of mRNA for this receptor. We developed a semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) protocol for measuring brain alpha 1b-adrenoceptor mRNA. The primers chosen yielded the predicted 409 base pair PCR product when used to amplify authentic alpha 1b-adrenoceptor cDNA. The identity of the RT-PCR products from rat brain was confirmed by restriction digest analysis and sequencing. Moreover, there was a good correlation between the levels of alpha 1b-adrenoceptor mRNA measured by RT-PCR in liver, whole brain and cerebellum with previous measurements using Northern blots and RNAse protection assays. We then performed RT-PCR on total RNA from hypothalamic-preoptic area tissue taken from ovariectomized control rats and from ovariectomized rats injected once or twice with 2 micrograms of estradiol benzoate at 24 or 24 and 48 h before sacrifice. Exposure to estradiol for either 24 or 48 h significantly increased levels of alpha 1b-adrenoceptor mRNA by 86-110% in the hypothalamus-preoptic area of ovariectomized female rats when compared to oil-treated controls. We also examined whether estradiol regulates alpha 1b-adrenoceptor mRNA in the cortex. Cortical alpha 1b-adrenoceptor mRNA levels were reduced to approximately 20% of control levels when measured 24 h after hormone injection. A similar decrease in cortical alpha 1b-adrenoceptor mRNA was observed 48 h after estrogen administration. In summary, estradiol treatment significantly increases the level of alpha 1b-adrenoceptor mRNA in the hypothalamus-preoptic area, a brain region involved in the control of reproductive function. In the cortex, a brain region with relatively few estrogen receptors, the same estrogen treatment reduces alpha 1b-adrenoceptor mRNA levels.

Animals↗
PubMed2002

Modulation Of [35S]-tert-butylbicyclophosphorothionate binding by somatostatin in rat hypothalamus.

1. The present study was designed to assess the effect of the tetradecapeptide somatostatin on the GABA(A) receptor complex in the rat hypothalamus. 2. GABA(A) receptors were labelled with [35S]-tert-butylbicyclophosphorothionate (TBPS), which binds in or near the chloride channel, and binding as assessed by in vitro quantitative autoradiography using a computer-assisted image analysis system. 3. Somatostatin inhibited the binding of [35S]-TBPS to the convulsant site of the hypothalamic GABA(A) receptor complex of rat slide-mounted hypothalamic structures in a concentration-dependent manner with an affinity in the micromolar range (10(-6) to 3 x 10(-6) mol/L). Somatostatin appeared to mimic the effects of the neurosteroid 5alpha-pregnane-3alpha ol-one (5alpha3alphaP), GABA and picrotoxin on [35S]-TBPS binding in the rat hypothalamus in all structures examined. Furthermore, GABA or muscimol (a GABA(A) receptor agonist), when added to the incubation medium, enhanced the capacity of somatostatin to inhibit [35S]-TBPS binding, with an IC50 of 10(-7) mol/L. However, incubation with bicuculline (a GABA(A) receptor antagonist) led to the abolition of the inhibitory effect of somatostatin on [35S]-TBPS specific binding in rat hypothalamus. 4. The present results demonstrate the presence of a modulatory effect of somatostatin on the GABA(A) receptor complex in rat hypothalamic structures. Furthermore, the data suggest that somatostatin allosterically modifies [35S]-TBPS binding through a mechanism similar to that of GABA. Taken together, these results provide evidence for the presence of somatostatin- GABA interactions in rat hypothalamus.

Animals↗
PubMed1998

Magnetic resonance imaging evaluation of the pituitary gland and hypothalamus in thalassaemic children with elevated serum ferritin levels.

OBJECTIVE: Despite modern treatment with hypertransfusion and chelation therapy, growth retardation continues to be observed in a significant proportion of thalassaemic children. The underlying reason remains unclear, but hypothalamic-pituitary axis disorder has been implicated. We aimed to assess iron overloading in the hypothalamus and pituitary gland in thalassaemic children with elevated serum ferritin, with and without growth retardation. METHODOLOGY: Twelve thalassaemic children on hypertransfusion and chelation therapy with high serum ferritin were investigated with magnetic resonance imaging (MRI). Five children, all over 10 years of age, had growth retardation. Gradient recalled echo sequence was used to highlight any susceptibility effect that could be due to iron in the hypothalamus or pituitary gland. RESULT: There was no evidence of abnormal hypointense signal in the hypothalamus or pituitary gland in the patients studied, regardless of the presence of growth retardation. CONCLUSION: There was no apparent characteristic MRI appearances of iron deposition in the hypothalamus or pituitary gland in thalassaemic children with high serum ferritin.

Adolescent↗
PubMed1999

Distribution of fibroblast growth factor-5 in rat hypothalamus, and its possible role as a regulator of feeding behaviour.

We previously reported that a transcript of fibroblast growth factor-5 (FGF-5) was more abundant in the brain of postnatal and adult mice than in the embryonic brain. This suggested that FGF-5 plays some role in the mature brain. Here, we have investigated the spatiotemporal expression and function of FGF-5 in the adult rat hypothalamus with the emphasis on feeding behaviour. In situ hybridization experiments demonstrated that, in both adequately fed and fasted (20 h) rats, FGF-5 transcripts were present within several nuclei in the hypothalamus (viz. the magnocellular part of the paraventricular nucleus, supraoptic nucleus, arcuate nucleus, median eminence, and ventromedial hypothalamic nucleus), but not in the lateral hypothalamic area. Quantitative detection of FGF-5 mRNA in the hypothalamus (especially in the paraventricular nucleus) indicated that food deprivation (20 h) reduced the expression of this gene to almost one-half of that seen in the control (fed) rats. The expression recovered to the control level after 1 h re-feeding, and this recovery persisted for several hours. Furthermore, FGF-5, when infused into the third ventricle, consistently reduced food intake, water intake and body weight gain, all in a dose-dependent manner. These results suggest that FGF-5 in the hypothalamus acts as a physiological regulator of feeding behaviour, and that its decreased expression during food deprivation may be important in stimulating appetite.

Animals↗
PubMed1976

Effect of subarachnoid haemorrhage on micro-circulation in hypothalamus and brain stem of dogs.

In order to investigate the relationship between cerebral vasospasm and microvasculature in the hypothalamus and brain stem, colloidal carbon was infused into the vertebral artery at various time intervals after experimental subarachnoid haemorrhage in dogs. Experiments which demonstrated vasospasm on angiogram were always accompanied by ischaemic changes in serial sections taken from the anterior hypothalamus to the brain stem. However, when it was demonstrated by angiography that the vasospasm had disappeared, the micro-circulation was restored to normal. Electron microscopy of the hypothalamus 48 hours and one week after subarachnoid haemorrhage, demonstrated swelling of the endothelial cells, enlargement of the perivascular glia and increase in number of the pinocytic vesicles in the cytoplasm, thus showing vasogenic oedema in this area. It is assumed that in addition to the vasogenic substance in extravasated blood, changes in irritability of cerebral vessels through the vasomotor pathways in the hypothalamus and brain stem might play an important role in the production of cerebral vasospasm.

Animals↗
PubMed1987

Effects of growth hormone-releasing hormone and corticotropin-releasing hormone on the release of thyrotropin-releasing hormone from the rat hypothalamus in vitro.

Effects of growth hormone-releasing hormone (GRH) and corticotropin-releasing hormone (CRH) on the release of immunoreactive thyrotropin-releasing hormone (ir-TRH) from the rat hypothalamus in vitro were studied. The rat hypothalamus was incubated in medium 199 with 1.0 mg/ml of bacitracin (pH 7.4) for 20 min. The amount of ir-TRH release into the medium was measured by radioimmunoassay. The ir-TRH release from the rat hypothalamus was inhibited significantly in a dose-related manner with the addition of GRH or CRH. These findings suggest that GRH and CRH inhibit ir-TRH release from the rat hypothalamus in vitro.

Animals↗
PubMed2001

Evidence of sex hormone binding globulin binding sites in the medial preoptic area and hypothalamus.

We have demonstrated a high density of both radiolabeled progesterone and estradiol conjugated to bovine serum albumin binding sites in the medial preoptic area and hypothalamus. Infusions of sex hormone binding globulin into the medial preoptic area of rats increased their female sexual receptivity similarly to the effect of estradiol conjugated to bovine serum albumin, suggesting sex hormone binding globulin acts at binding sites for estradiol conjugated to bovine serum albumin. In this study sex hormone binding globulin was used to displace radiolabeled progesterone conjugated to bovine serum albumin from plasma membrane fractions from the medial preoptic area-anterior hypothalamus and medial basal hypothalamus of ovariectomized rats injected with either 5 microg estradiol benzoate or sesame oil vehicle. We found that sex hormone binding displaced radiolabeled progesterone conjugated to bovine serum albumin in both areas and that in vivo estradiol treatment greatly increased the relative displacement by sex hormone binding globulin in the medial preoptic area-anterior hypothalamus. We interpret these data as indicating the presence of sex hormone binding globulin receptors in brain plasma membranes and further suggest that endogenous steroid conditions may alter these receptors.

Animals↗
PubMed2006

Expression of glucose-6-phosphatase system genes in murine cortex and hypothalamus.

The glucose-6-phosphatase (G6Pase) system participates in the regulation of glucose homeostasis by converting glucose-6-phosphate (G6P) into glucose and inorganic phosphates. We have used an RT-PCR-based cloning and sequencing approach to study the expression of components of the G6Pase system in the hypothalamus and cortex tissues of the ob/ob mouse. We observed the expression of hepatic G6Pase catalytic subunit, G6PC, in both tissues, although increased template inputs were required for its detection. Conversely, expression of both the mouse homologue of the previously-described brain-specific G6P translocase T1 (G6PT1) variant and of the hepatic G6PT1 isoform was easily detectable in hypothalamus and cortex tissues. Of the proposed G6Pase catalytic subunit homologues, the expression of murine ubiquitous G6Pase catalytic subunit-related protein (UGRP, G6PC3) was also easily detectable in both tissues. However, islet-specific G6Pase catalytic subunit-related protein (IGRP, G6PC2) was expressed in a tissue-specific manner, and was detectable only in hypothalamus tissue at increased template inputs. We conclude that cells within ob/ob mouse hypothalamus and cortex tissues express genes with either established or proposed roles in G6P hydrolysis.

Animals↗
PubMed2006

Expression of corticosterone-binding globulin in the rat hypothalamus.

We observed coexistence of corticosteroid-binding globulin (CBG) with vasopressin (VP) and oxytocin (OT) in magnocellular neurons in rat hypothalamus by combined immunoperoxidase staining and immunofluorescence. A portion of the supraoptic and of the paraventricular neurons showed double immunostaining of CBG with either VP or with OT. CBG staining was intensified by pretreating animals with colchicine to block axonal transport. CBG was also observed in widespread axonal projections throughout the lateral hypothalamus, the median eminence and the posterior pituitary lobe. Single ependymal cells and some of the endocrine cells in the anterior lobe contained specific CBG immunoreactivity. IN SITU hybridization of semithin sections with a synthetic oligonucleotide probe to CBG mRNA provided staining of magnocellular hypothalamic neurons, but not ependymal cells or anterior lobe cells. Western blots of CBG extracted by affinity chromatography from hypothalamus homogenates showed a band at approximately 50 kDa. Our observations indicate the intrinsic expression of CBG in peptidergic hypothalamus neurons in rat. The multiple locations of CBG-expressing neurons indicate multiple functional properties, probably exceeding the role of a mere steroid transporter. CBG is likely to be subject to axonal transport and secretion in a neuropeptide-like fashion, perhaps involved in neuroendocrine regulation, which may include stress responses.

Animals↗
PubMed1981

Influence of the hypophysio-adrenocortical system on the metabolism of 3H-adrenaline in the hypothalamus, hypophysis and the rest of the brain of rats.

Possible correlation between modified state of the adrenocortical system and the metabolic fate of 3H-adrenaline in central regions was studied. The formation of 3H-acid metabolites from 3H-adrenaline showed high increase in brain and hypothalamus of hypophysectomized rats from the value of normal animals. Adrenalectomy was also found to be associated with increased acid metabolite formation in the whole of the brain. Preadministration of metopirone increased formation of acid metabolites in the hypothalamus and hypophysis of normal rats. The transformation of radioactive normetanephrine was significantly higher in the hypothalamus of rats administered with elliptone as well as with metopirone. The hypophysis showed increase in metanephrine formation only by pretreatment with elliptone. Brain tissue demonstrated increased rate of normetanephrine formation after adrenalectomy and hypophysectomy. Hypophysectomy increased physiological accumulation of 3H-adrenaline in all the three regions studied but the maximal effect was observed in the hypothalamus. The preadministration of elliptone and metopirone decreased accumulation of labeled adrenaline in the brain and hypophysis of normal rats. The results suggest that inactivation of adrenocortical system either pharmacologically or physiologically leads to activation of the the processes of catecholamine metabolic degradation whereas the physiological accumulation of adrenaline slows down and this conclusion is valid for a great majority of observations presented in this study.

Adrenalectomy↗
PubMed1985

Glucostatic regulation of (+)-[3H]amphetamine binding in the hypothalamus: correlation with Na+,K+-ATPase activity.

Preincubation of rat hypothalamic slices in glucose-free Krebs-Ringer buffer (37 degrees C) resulted in a time-dependent decrease in specific (+)-[3H]amphetamine binding in the crude synaptosomal fraction prepared from these slices. The addition of D-glucose resulted in a dose- and time-dependent stimulation of (+)-[3H]amphetamine binding, whereas incubation with L-glucose, 2-deoxy-D-glucose, or 3-O-methyl-D-glucose failed to increase the number of (+)-[3H]amphetamine binding sites. Ouabain potently inhibited the glucose-induced stimulation of (+)-[3H]amphetamine binding, suggesting the involvement of Na+,K+-ATPase. Preincubation of hypothalamic slices with glucose also resulted in an increase in Na+,K+-ATPase activity and the number of specific "high-affinity" binding sites for [3H]ouabain, and a good correlation was observed (r = 0.89; P less than 0.02) between the glucose-stimulated increase in (+)-[3H]amphetamine and [3H]ouabain binding. Similar increases in (+)-[3H]amphetamine binding, [3H]ouabain binding, and Na+,K+-ATPase activity were observed in the hypothalamus after parenteral administration of glucose to rats. The administration of anorectic doses of amphetamine (0.1-5.0 mg/kg of body weight) also increased Na+,K+-ATPase activity in the hypothalamus. These data suggest that the (+)-[3H]amphetamine binding site in hypothalamus, previously linked to the anorectic actions of various phenylethylamines, is regulated both in vitro and in vivo by physiological concentrations of glucose. Glucose and amphetamine appear to interact at common sites in the hypothalamus to stimulate Na+,K+-ATPase activity, and the latter may be involved in the "glucostatic" regulation of appetite.

Animals↗