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At least 1,117 records · Page 62Linked to original sources
PubMed2000

Noradrenaline systems in the hypothalamus, amygdala and locus coeruleus are involved in the provocation of anxiety: basic studies.

A variety of stressful events, including emotional stress, cause a marked increase in noradrenaline release in several brain regions, and especially in the hypothalamus, amygdala and locus coeruleus, in the rat brain. These findings suggest that an increased noradrenaline release could be closely related to the provocation of negative emotions such as anxiety and/or fear. In order to confirm this hypothesis, we carried out several studies. Diazepam, a typical benzodiazepine anxiolytic, significantly attenuated not only the immobilization stress-induced increase in noradrenaline release in the three rat brain regions but also the emotional changes of these animals, and these effects were antagonized by flumazenil, a benzodiazepine antagonist. Naloxone and opioid agents, such as morphine, beta-endorphin and [Met(5)]-enkephalin, significantly enhanced and attenuated the stress-induced increase in noradrenaline release in these regions and the stress-induced emotional change, respectively. Two stressful events which predominantly involve emotional factors, i.e., psychological stress and conditioned fear, caused significant increases in noradrenaline release selectively in these three brain regions and these increases were also significantly attenuated by pretreatment with diazepam in a flumazenil reversible manner. Yohimbine, an alpha(2)-adrenoceptor antagonist which caused a marked increase in noradrenaline release in the several brain regions, had an anxiolytic action in the two behavioral tests involving anxiety, i.e., the conditioned defensive burying test and the modified forced swim test. beta-Carbolines, which possess anxiogenic properties, significantly increased noradrenaline release in the hypothalamus, amygdala and locus coeruleus. Taken together, these findings suggest that the increased release of noradrenaline in the hypothalamus, amygdala and locus coeruleus is, in part, involved in the provocation of anxiety and/or fear in animals exposed to stress, and that the attenuation of this increase by benzodiazepine anxiolytics acting via the benzodiazepine receptor/GABAA receptor/chloride ionophore supramolecular complex may be the basic mechanism of action of these anxiolytic drugs.

Amygdala↗
PubMed1997

Pretreatment with 5-HT1A receptor agonist flesinoxan attenuates Fos protein in rat hypothalamus.

The 5-HT1A receptor agonist flesinoxan has anxiolytic activity and concurrently enhances plasma corticosterone levels in rats. After a second injection of flesinoxan 24 h later, the corticosterone response disappears, but not the anxiolytic effects. Male rats received two injections with either flesinoxan or vehicle within 24 h. Flesinoxan challenge enhanced Fos immunoreactivity in the paraventricular nucleus of the hypothalamus, the central amygdala, and the dorsolateral part of the bed nucleus of the stria terminalis and plasma corticosterone levels in the vehicle-pretreated rats. Flesinoxan pretreatment resulted in an attenuated response of plasma corticosterone levels and Fos-positive neurons in the paraventricular nucleus of the hypothalamus, but not in the central amygdala and the bed nucleus after a flesinoxan challenge. The differential desensitization levels for both behaviour and neuroendocrine responses after flesinoxan treatment seem to correspond to different organization levels in the brain, like limbic system and hypothalamus.

Animals↗
PubMed1997

delta 9-Tetrahydrocannabinol increases proopiomelanocortin gene expression in the arcuate nucleus of the rat hypothalamus.

delta 9-Tetrahydrocannabinol, the main psychoactive component of cannabis, produces a large spectrum of pharmacological effects, many of which have been linked to interaction with the opioid system. The aim of this study was to examine the effects of delta 9-tetrahydrocannabinol on proopiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus and anterior lobe of the pituitary. We report, for the first time, that a 5-day treatment with delta 9-tetrahydrocannabinol (5 mg/kg per day, i.p.) increased (38%) POMC mRNA levels in the arcuate nucleus of the hypothalamus but was without effect in the anterior lobe of the pituitary. These data indicate that delta 9-tetrahydrocannabinol stimulates opioid gene expression and regulates distinctively POMC in the hypothalamus and the anterior lobe of the pituitary in the rat.

Animals↗
PubMed1999

Methamphetamine alters prodynorphin gene expression and dynorphin A levels in rat hypothalamus.

Chronic administration of morphine or cocaine affects opioid gene expression. To better understand the possible existence of common neuronal pathways shared by different classes of drugs of abuse, we studied the effects of methamphetamine on the gene expression of the opioid precursor prodynorphin and on the levels of peptide dynorphin A in the rat brain. Acute (6 mg/kg, intraperitoneally, i.p.) and chronic (6 mg/kg, i.p. for 15 days) methamphetamine markedly raised prodynorphin mRNA levels in the hypothalamus, whereas no effect was observed in the hippocampus. Dynorphin A levels increased after chronic treatment in the hypothalamus and in the striatum, whereas no significant changes were detected after acute treatment. These results indicate that methamphetamine affects prodynorphin gene expression in the hypothalamus, which may be an important site (also for its relevant neuroendocrine correlates) for opioidergic mechanisms activated by addictive drugs.

Animals↗
PubMed2003

Photostimulated fos-like immunoreactivity in tuberal hypothalamus of photosensitive vs. photorefractory turkey hens.

Photorefractoriness in commercial turkey hens can be viewed as a failure of previously sexually stimulatory photoperiods to maintain egg production via activation of cGnRH I neurons, but the neural locus of photorefractoriness, i.e., where in the brain failure occurs, is not known. We used a c-fos antiserum that detects c-Fos and Fos-related antigens to characterize Fos-like immunoreactivity (FLI) as a measure of neuronal activation. FLI was measured in somatically mature, photosensitive hens (held on short photoperiods [8L:16D] for at least 10 weeks) before (non-photostimulated-photosensitive group) and after 48 h of exposure to long photoperiods (16L:8D; photostimulated-photosensitive group). We also measured FLI in hens that had become photorefractory, transferred to short photoperiods for 1 week--an insufficient time period to reverse photorefractoriness--and then exposed to long photoperiods for 48 h (photostimulated-photorefractory group). FLI was nearly absent in the tuberal hypothalamus of non-photostimulated-photosensitive hens but FLI was abundant in photostimulated-photosensitive hens. FLI was greatly reduced (P<0.01) in the rostral tuberal hypothalamus of photostimulated-photorefractory hens. All hens showed variable extra-tuberal FLI in locations associated with stress, e.g., paraventricular nucleus, lateral septal area, and nucleus taenia. Double-label fluorescence immunohistochemistry with c-fos antiserum and anti-Neu-N, a neuron-specific protein, showed that a substantial fraction of tuberal FLI-positive cells in photostimulated-photosensitive hens were neuronal. These results implicate neurons in the rostral tuberal hypothalamus as a potential neural locus of photorefractoriness, as FLI in this region appears coupled with cGnRH I activation in photostimulated-photosensitive but not photostimulated-photorefractory turkey hens.

Animals↗
PubMed1998

Glucose-6-phosphatase activity in the hypothalamus of the ob/ob mouse.

The hypothalamus and cortex from ob/ob mice and their lean littermates were sonicated and then incubated with glucose-6-phosphate (glucose-6-P) and glycerol phosphate (glycerol-P). The difference between the rates of hydrolysis of glucose-6-P and glycerol-P was taken as the measure of glucose-6-phosphatase activity. The activity was much higher in the hypothalamus from ob/ob mice versus their lean littermates. Activity was undetected in the cortex. These findings raise the possibility that a defect in the regulation of glucose-6-phosphatase activity in a portion of the hypothalamus may relate to the mechanism underlying obesity in the ob/ob mouse. However, obese gene product administration to ob/ob mice, while reducing the body weight, did not alter the glucose-6-phosphatase activity.

Animals↗
PubMed1997

Histamine release from the hypothalamus induced by gravity change in rats and space motion sickness.

Freely moving rats were exposed to 2 g hypergravity in an animal centrifuge device to produce motion sickness. Histamine release from the anterior hypothalamus of the rats was measured in vivo with a microdialysis technique. After a 2-h load of 2 g hypergravity, rats ate kaolin. Because pica, eating a nonnutritive substance such as kaolin, is a behavioral index of motion sickness in rats, this finding indicates that the rats suffered from motion sickness. During 2 g hypergravity for 2-h, histamine release from the hypothalamus was transiently increased. In contrast, neither the transient increase of histamine release nor the kaolin consumption were induced by 2 g hypergravity in bilaterally labyrinthectomized rats. Pretreatment with alpha-fluoromethylhistidine, an inhibitor of histamine-synthesizing enzyme, decreased both the basal and hypergravity-induced releases of histamine from the hypothalamus and suppressed the kaolin consumption induced by hypergravity. Taken together, these findings suggest that the vestibular information of changes in gravity activate the histaminergic neuron system, resulting in the development of motion sickness. More prolonged stimulation, a 4-h load of 2 g hypergravity, induced significant increase of kaolin consumption on postdays 1-3, though rats ate kaolin on postdays 1-2 after 2 g hypergravity for 2 h. During 2 g hypergravity for 4 h, the initial transient increase of histamine release was followed by the gradual increase of histamine release after the end of centrifugation. It is suggested that rats adapted to the hypergravity environment after centrifugation for 4 h, but not 2 h, so that the change in gravity from 2 g to 1 g became a provocative stimulation. We, therefore, concluded that motion sickness in rats induced by a negative change in gravity can be used as a simulation of space motion sickness, which is induced by exposure to microgravity. Histaminergic activation in the development of motion sickness induced by negative change in gravity might be an underlying mechanism of space motion sickness.

Animals↗
PubMed1975

In vitro metabolism of 3-H-androstenedione by the male rat pituitary, hypothalamus, and hippocampus.

The in vitro metabolism of 2,2-3-H-androstenedione by the pituitary, hypothalamus, and hippocampus of intact and castrated adult male rats was studied. Conversion of androstenedione to radiochemically pure 5alpha-androstanedione, testosterone, 5alpha-dihydrotestosterone, androsterone, and traces of 3alpha, 5alpha-androstanediol was demonstrated in minced preparations of the three tissues in the absence of cofactors. 5alpha-androstanedione was the metabolite formed in the highest proportion. The pituitary showed the highest enzymatic conversions followed in decreasing order by the hippocampus and the hypothalamus. Castration performed three weeks prior to the experiments resulted in a significant decrease of pituitary 17beta-old-dehydrogenase activity with a concomitant increase of 5alpha-reductase. No significant changes were observed after castration in the hypothalamus and the hippocampus.

Androstenedione↗
PubMed1996

The distribution of estrogen receptor-beta mRNA in the rat hypothalamus.

The recent cloning of a second form of the estrogen receptor (ER-beta) has made it possible to map the distribution of ER-beta mRNA-containing perikarya in the rat hypothalamus. The present in situ hybridization histochemical studies have detected ER-beta mRNA in the medial preoptic area; the anterior periventricular, paraventricular, supraoptic, arcuate, medial tuberal and medial mammillary nuclei; the bed nucleus of the stria terminals, and zona incerta. As previously described for the classical ER (ER-alpha) mRNA, a dense accumulation of ER-beta mRNA-expressing perikarya is present in the medial preoptic area and bed nucleus of the stria terminalis. In contrast, ER-beta mRNA was also concentrated in the paraventricular and supraoptic nuclei, brain regions which contain little or no ER-alpha mRNA. Moreover, the arcuate and ventromedial nuclei, areas with abundant ER-alpha. contain only a weak level of ER-beta hybridization signal. The description of ER-beta mRNA-containing perikarya in the rat hypothalamus provides a foundation for further morphological and physiological studies aimed at elucidating the role of ER-beta in the hypothalamus.

Animals↗
PubMed2002

Leptin and melanocortin signaling in the hypothalamus.

The regulation of body weight in humans is coordinated by the interplay between food intake and energy expenditure. The identification of the adipocyte-secreted hormone leptin as a key regulator on both of these processes has shed new light on the pathways involved in their regulation. Indeed, mutations in the gene's encoding leptin and its cognate receptor cause severe obesity in humans. Leptin's actions are mediated principally by target neurons in the hypothalamus where it acts to alter food intake, energy expenditure, and neuroendocrine-function. Recently, it has become clear that a number of critical neuropeptides are regulated by leptin in the hypothalamus. Among these is the proopiomelanocortin (POMC)-derived peptide, alpha-melanocyte-stimulating hormone (alpha-MSH), which is produced in the arcuate nucleus and is a potent negative regulator of food intake. Like leptin, mutations in POMC or in central melanocortin receptors lead to obesity in humans. Thus, an understanding of the mechanisms by which the leptin and melanocortin pathways signal in the hypothalamus is critical in order to begin to clarify the pathways involved in regulating body weight in humans.

Agouti-Related Protein↗
PubMed1996

CGRP in the trigeminal nucleus, spinal cord and hypothalamus: effect of gonadal steroids.

Calcitonin gene-related peptide (CGRP) contents were assayed in cervical spinal cord, trigeminal nucleus and hypothalamus throughout the estrous cycle and in male and ovariectomized rats. In the trigeminal nucleus, neither testosterone nor 17 beta-estradiol seem to affect CGRP accumulation, but progesterone seems to decrease it. In the cervical spinal cord, ovarian steroids seem to decrease CGRP while testosterone does not seem to influence it. In the hypothalamus, CGRP was only detectable in the male rat suggesting a positive effect of testosterone. It had marked circadian rhythm. In conclusion, CGRP content appears to be affected by gonadal steroids in the hypothalamus, the cervical spinal cord and the trigeminal nucleus in the rat.

Animals↗
PubMed1998

The hypothalamus: cross-roads of endocrine and behavioural regulation in grooming and aggression.

Anatomical and functional studies show that the hypothalamus is at the junction of mechanisms involved in the exploratory appraisal phase of behaviour and mechanisms involved in the execution of specific consummatory acts. However, the hypothalamus is also a crucial link in endocrine regulation. In natural settings it has been shown that behavioural challenges produce large and fast increases in circulating hormones such as testosterone, prolactin, corticotropin and corticosterone. The behavioural function and neural mechanisms of such fast neuroendocrine changes are not well understood. We suggest that behaviourally specific hypothalamic mechanisms, at the cross-roads of behavioural and endocrine regulation, play a role in such neuroendocrine changes. Mild stimulation of the hypothalamic aggressive area, produces stress levels of circulating prolactin, corticotropin, and corticosterone. Surprisingly luteinizing hormone does not change. This increase in stress hormones is due to the stimulation itself, and not caused by the stress of fighting. Similar increases in corticosterone are observed during electrical stimulation of the hypothalamic self-grooming area. The corticosterone response during self-grooming-evoking stimulation is negatively correlated with the amount of self-grooming observed, suggesting that circulating corticosterone exerts a negative feedback control on grooming. Earlier literature, and preliminary data form our laboratory, show that circulating corticosterone exerts a fast positive feedback control over brain mechanisms involved in aggressive behaviour. Such findings suggest that the hormonal responses caused by the activity of behaviourally specific areas of the hypothalamus may be part of a regulation mechanism involved in facilitating or inhibiting the very behavioural responses that can be evoked from those areas. We suggest that studying such mechanisms may provide a new approach to behavioural dysfunctions associated with endocrine disorders and stress.

Aggression↗
PubMed2000

IL-1beta immunoreactive neurons in the human hypothalamus: reduced numbers in multiple sclerosis.

Corticotropin-releasing hormone (CRH)-containing neurons in the paraventricular nucleus (PVN) in the hypothalamus of multiple sclerosis (MS) patients are hyperactivated. Since interleukin-1 (IL-1)beta is a powerful activator of CRH neurons, its immunohistochemical expression was studied in the postmortem hypothalamus of MS patients (n=11) and matched controls (n=11). Hypothalamic tissue of 10/11 MS patients showed demyelinating lesions that in many cases contained IL-1beta-immunoreactive (ir) macrophages and glial cells. In control subjects IL-1beta-ir was only sporadically found in glial cells. Interestingly, abundant IL-1beta-ir was also present in hypothalamic neurons. Neuronal IL-1beta co-localised with oxytocin and not with vasopressin or CRH. IL-1beta clearly yielded a less intense staining in neurons and numbers of IL-1-ir neurons in the PVN were 4.5-fold reduced in MS. We suggest that IL-1beta produced by activated glial cells in the hypothalamus of MS patients may contribute to the activation of the hypothalamic CRH neurons, while reduced expression of neuronal IL-1beta in MS patients may have consequences for neuroendocrine, behavioural or autonomic functioning.

Adult↗
PubMed1998

Effect of IL-1alpha on the release of norepinephrine in rat hypothalamus.

The increased release of norepinephrine (NE) in the brain as part of the 'acute phase response' has been postulated to result from a direct action of IL-1 on the hypothalamus. To test whether the effects of IL-1alpha were direct, we carried out in vivo experiments using microdialysis and measured NE release in the hypothalamus using high pressure liquid chromatography (HPLC). Two groups of male Sprague Dawley rats were either injected intraperitoneally with 1 ml of IL-1alpha (2 microg/ml) or had IL-1alpha 2 microl (100 ng/ml) infused directly into the medial hypothalamus. A significant increase in extracellular hypothalamic NE was observed in the animal group treated with IL-1alpha intraperitoneally and not in the controls or the group treated with IL-1alpha intracerebrally. One-way ANOVA showed a significant effect of drug and route of administration with the ip IL-1alpha treated group, differing from all other groups (vehicle ip, IL-1alpha ic, and vehicle ic). Therefore these findings suggest that some aspects of IL-1alpha actions on the HPA may be indirect requiring other intermediate steps or mediators outside the central nervous system.

Animals↗
PubMed1998

NPY messenger RNA is increased in medial hypothalamus of anorectic tumor-bearing rats.

Previous investigations suggest that neuropeptide Y (NPY) feeding mechanisms and corticotropin releasing factor (CRF) are altered in anorectic tumor-bearing (TB) rats. To better determine the relationship of NPY and CRF synthesis to cancer anorexia we measured mRNA for these peptides in medial and lateral hypothalamus of TB and control rats. NPY and CRF mRNA were reliably detected by Northern blot analysis only in medial hypothalamus, where NPY message was elevated significantly in TB rats. CRF mRNA tended to be reduced in both pair-fed (PF) and TB rats, but did not reach statistical significance. Concentrations of NPY or CRF were not altered significantly in either the lateral or medial hypothalamus of TB or PF rats. These results suggest that the transcription of NPY is elevated in PF rats and is increased further in anorectic TB rats. The lack of significant increases in levels of peptides may be related to dilution, due to measuring a relatively large block of hypothalamic tissue. Alternatively, translation of the signal for NPY production may be inhibited, or degradation of peptide levels may be increased.

Animals↗
PubMed2000

Collateral projection from the amygdalo--hippocampal transition area and CA1 to the hypothalamus and medial prefrontal cortex in the rat.

Amygdaloid and hippocampal neurons projecting to both the medial prefrontal cortex and hypothalamus by way of axon collaterals were examined in the rat by double labeling method using fluorescence retrograde tracers. Fluoro-gold was injected in the medial prefrontal cortex, while Fluoro-red was injected into the ventromedial and ventral premammillary nuclei of the hypothalamus. The results indicated that neurons which sent axon collaterals to both the medial prefrontal cortex and hypothalamus constituted 50 or 30% of populations of medial prefrontal cortex-projecting neurons in the amygdalo-hippocampal transition area or in CA1, respectively. Possible roles of the neurons with axon collaterals in sexually related aggressive and/or defensive behavior were discussed.

Amygdala↗
PubMed2003

Morphological study of orexin neurons in the hypothalamus of the Long-Evans rat, with special reference to co-expression of orexin and NADPH-diaphorase or nitric oxide synthase activities.

Orexins, novel neuropeptides, are exclusively localized in the hypothalamus and implicated in the regulation of a variety of activities, including food intake and energy balance. Nitric oxide (NO), an unconventional neurotransmitter, is widely present in numerous brain regions including the hypothalamus, and has similar physiological roles to those of the orexins. The present study was undertaken to examine the distribution of orexin neurons and the presence of neuronal nitric oxide synthase (nNOS) in the orexin neurons to clarify whether NO interacts with the orexins in the neuronal regulation activities in the Long-Evans rat. We used two double-labeling methods: nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry in combination with orexin immunohistochemistry, and double-labeling fluorescent immunohistochemistry for orexin and nNOS. The majority of the orexin immunoreactive neurons were localized mainly in the areas of the dorsomedial hypothalamic nucleus (DMN), the dorsal part of the perifornical nucleus (PEF) and lateral hypothalamic area. The orexin immunoreactive cell bodies were medium in size, and triangular, round, elliptic, and fusiform in shape. The sizes and shapes of orexin neurons in the different parts were similar. Cell bodies coexpressing the orexin and nNOS or NADPH-d were present in the areas of the DMN and the PEF, and the nerve fibers containing orexin and nNOS were distributed in the DMN and PEF, arcuate nucleus (ARN) and ventromedial hypothalamic nucleus (VMH). These results provide morphological evidence that there exists a population of nNOS- or NADPH-d-/orexin-coexpressing neurons in the orexinergic cell group in the hypothalamus, and taken together with previous findings, suggest that NO may play a role in the mechanisms by which orexin neurons regulate food intake and energy balance.

Animals↗
PubMed2001

Chronic exercise increases GAD gene expression in the caudal hypothalamus of spontaneously hypertensive rats.

Previous studies have suggested that a gamma-amino-butyric acid (GABA) deficit in the caudal hypothalamus (CH) of the spontaneously hypertensive rat (SHR) contributes to elevated levels of arterial pressure. The purpose of this study was to examine if SHR that underwent exercise training demonstrated a blunted development of hypertension and greater levels of glutamic acid decarboxylase (GAD) mRNA transcripts in the caudal hypothalamus. SHR were randomly paired and assigned to either a trained group (T; n=9) or a non-trained control group (NT; n=9). Trained animals were exercised for 10 weeks on a motorized treadmill while NT animals concurrently rested on a mock-treadmill. Following the 10-week training period, Northern blot analyses of mRNA for both the 65-kDa (GAD(65)) and 67-kDa (GAD(67)) isoforms of GAD were performed on tissue from caudal hypothalamic and cerebellar control brain regions. Exercise training simultaneously blunted the developmental rise in blood pressure in SHR (Delta59+/-9 mmHg in trained versus Delta77+/-9 mmHg in non-trained; P<0.03) and increased both GAD(65) (147+/-44%) and GAD(67) (162+/-77%) mRNA transcript levels in the CH (P<0.05). In contrast, no difference was detected in GAD mRNA levels in the cerebellum between T and NT SHR. These findings are consistent with our previous functional studies and demonstrate that exercise can significantly and specifically upregulate GAD gene transcript levels in the caudal hypothalamus of hypertensive rats.

Animals↗