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PubMed2006

Beacon-like immunoreactivity in the hypothalamus of domestic chick.

Beacon-immunoreactive (B-ir) fibres and neurons in the hypothalamus of the domestic chick (Gallus domesticus) were studied using an immunohistochemical technique in order to verify the presence and elucidate the pattern of distribution of this novel peptide in an avian brain. B-ir neurons were seen in the n. supraopticus, pars ventralis and pars externus; n. magnocellularis preopticus, pars dorsalis, medialis and ventralis; n. preopticus periventricularis; n. suprachiasmaticus, pars medialis; n. ventrolateralis thalami. Only few B-ir cells were scattered in the most anterior part of the lateral hypothalamic area. B-ir fibres, appearing as thin punctuate structures, were seen mainly along the walls of the third ventricle and in the ventromedial hypothalamus. Labelled fibres and terminals were located in the external and internal zones of the anterior and posterior median eminence. In particular, fibre terminals were seen close to the capillary loops of the hypothalamo-hypophysial portal system. The anatomical data of the present study regarding the distribution of B-ir in the chick hypothalamus suggest that beacon may play a key role in the regulation of the neuroendocrine system by acting as a neuromodulator and/or neurotransmitter.

Animals↗
PubMed1989

Changes in met-enkephalin and beta-endorphin contents in the hypothalamus and the pituitary in diabetic rats: effects of insulin therapy.

1. Immunoreactive (IR)-met-enkephalin and beta-endorphin contents in the hypothalamus and the pituitary were measured in alloxan-diabetic rats with or without insulin treatment. 2. Both IR-met-enkephalin and IR-beta-endorphin in the pituitary were substantially reduced in alloxan-diabetic rats 1 month after treatment. 3. Hypothalamic IR-beta-endorphin content was also significantly lower. 4. Gel-filtration chromatography showed that the peaks co-eluting with met-enkephalin precursor, met-enkephalin and beta-endorphin were lower in the pituitaries from the diabetic rats, whereas the peaks co-eluting with beta-endorphin precursor and beta-lipotropin were not. 5. In another experiment, the IR-beta-endorphin contents of the neuro-intermediate lobe and hypothalamus, but not the anterior lobe were significantly lowered in diabetic rats, whereas IR-met-enkephalin contents were significantly reduced in both the anterior and neuro-intermediate lobe. 6. All these changes were reversed by insulin treatment. 7. As a decrease in general protein synthesis could not explain the recorded changes, these results suggest a possible direct role of insulin in regulating the opioid peptide content of the hypothalamus and pituitary.

Animals↗
PubMed1991

Effect of reserpine on catecholamine contents and met-enkephalin and beta-endorphin levels in the hypothalamus and the pituitary.

1. The effects of reserpine treatment on the contents of catecholamines and opioid peptides have been studied in the rat hypothalamus and pituitary. 2. Hypothalamic and pituitary catecholamines were drastically depleted following acute reserpine treatment. 3. Reserpine treatment also resulted in a significant decrease in immunoactive met-enkephalin content in both the hypothalamus (25%) and the anterior lobe (50%), but not in the neurointermediate lobe of the pituitary. 4. No changes were observed in immunoactive beta-endorphin levels. 5. These findings suggest that the met-enkephalin contents in the hypothalamus and the anterior pituitary may be under catecholaminergic control. 6. The lack of effect of acute reserpine treatment on immunoactive beta-endorphin contents might be due to the opposing effects of adrenergic and dopaminergic mechanisms.

Animals↗
PubMed1995

Synergistic effects of Bay K 8644 and bradykinin on norepinephrine release in the hypothalamus of spontaneously hypertensive rats.

1. In the present study, we examined the effects of Bay K 8644, a dihydropyridine (DHP)-sensitive Ca2+ channel agonist, and bradykinin on norepinephrine release in the hypothalamus of spontaneously hypertensive rats (SHR). 2. In the preliminary studies using Sprague-Dawley rats, Bay K 8644 by itself had no significant effects on the stimulation-evoked [3H]-norepinephrine release from hypothalamic slices. Bradykinin increased the stimulation-evoked [3H]-norepinephrine release in a dose-related fashion. The facilitatory effects of bradykinin on norepinephrine release were potentiated by Bay K 8644. 3. In SHR, Bay K 8644 significantly increased the stimulation-evoked norepinephrine release from hypothalamic slices. However, exposure of slices to Bay K 8644 caused no significant effects on norepinephrine release in Wistar-Kyoto (WKY) rats. The effects of Bay K 8644 in combination with bradykinin on the stimulation-evoked norepinephrine release were also greater in SHR than in WKY rats. 4. These results demonstrate that Bay K 8644 significantly potentiated the facilitatory effects of bradykinin on norepinephrine release in rat hypothalamus. The finding indicates a possible interaction of bradykinin with DHP-sensitive Ca2+ channels in the central nervous system. Furthermore, the pronounced effects of Bay K 8644 and bradykinin in SHR suggest that bradykinin-related Ca2+ channels might have a role in the regulation of norepinephrine release in the hypothalamus of SHR.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

5-HT1A receptor agonist flesinoxan enhances Fos immunoreactivity in rat central amygdala, bed nucleus of the stria terminalis and hypothalamus.

5-Hydroxytryptamine-1A (5-HT1A) receptor agonists, including flesinoxan, reduce anxiety and activate the hypothalamus-pituitary-adrenal (HPA) axis under basal conditions. In order to investigate the underlying neural mechanisms we investigated immunoreactivity for the immediate early gene protein product Fos (Fos-ir) in rat brains 1 h after flesinoxan treatment (0.0, 0.3 or 3.0 mg/kg p.o.). Typically, 5-HT1A receptor-containing brain areas, such as the dorsal raphe nuclei, hippocampus, septum, diagonal band and the cortical and basomedial amygdala, do not show Fos-ir. Apparently, binding of flesinoxan at the 5-HT1A receptor does not directly lead to activation of c-fos in the cell, probably due to its negative coupling to adenylate cyclase. However, in typically non-5HT1A receptor-containing brain areas Fos-ir is increased due to flesinoxan treatment, as in the paraventricular nucleus of the hypothalamus (PVN), the dorsolateral part of the bed nucleus of the stria terminalis (BNSTdl) and the central amygdala (CeA). Flesinoxan-treated rats also exhibited higher plasma corticosterone levels than vehicle-treated animals, which suggests the involvement of corticotropin-releasing hormone (CRH) or vasopressin in the hypothalamus. After double immunolabelling (Fos/CRH or Fos/vasopressin), every CRH neuron detected in the PVN also contained Fos. Moreover, a significant correlation existed between the number of Fos-ir neurons in the PVN and the plasma corticosterone level. Hardly any Fos/vasopressin double labelling was visible in the PVN. Accordingly, flesinoxan exerts its activating effects on the HPA axis via CRH neurons in the PVN. These effects are trans-synaptically mediated by other brain areas, such as the CeA and BNSTdl, which also show increased Fos-ir.

Amygdala↗
PubMed2004

Chronic stress attenuates GABAergic inhibition and alters gene expression of parvocellular neurons in rat hypothalamus.

Chronic stress causes disinhibition of the hypothalamus-pituitary-adrenal axis. Consequently, the brain is overexposed to glucocorticoids which in humans may precipitate stress-related disorders, e.g. depression. The hypothalamus-pituitary-adrenal activity is strongly regulated by GABAergic input to parvocellular neurons in the hypothalamic paraventricular nucleus. We here report a reduced frequency of miniature inhibitory postsynaptic currents (mIPSCs) in parvocellular neurons of rats exposed to 3 weeks of unpredictable stress. The mIPSC amplitude and kinetic properties were unchanged, pointing to a presynaptic change caused by chronic stress. Because paired-pulse inhibition was unaffected by chronic stress, the number of functional GABAergic synaptic contacts rather than the release probability seems to be reduced after chronic stress. Linearly amplified RNA from postsynaptic cells was hybridized with multiple cDNA clones of interest, including most GABA(A) receptor subunits. In agreement with the electrophysiological observations, relative expression of the prevalent GABA(A)alpha1, alpha3, gamma1 and gamma2 receptor subunits, which largely contribute to the recorded responses, was not altered after chronic stress. However, expression of the extra-synaptic GABA(A)alpha5 subunit, earlier linked to depression in humans, and of the delta receptor subunit were found to be significantly changed. In conclusion, chronic stress leads to presynaptic functional alterations in GABAergic input to the paraventricular nucleus which could contribute to the observed disinhibition of the hypothalamus-pituitary-adrenal axis; additionally other aspects of GABAergic transmission may also be changed due to transcriptional regulation of specific receptor subunits in the parvocellular neurons.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2005

Forebrain projections to the hypothalamus are topographically organized in anurans: conservative traits as compared with amniotes.

The organization of the forebrain in amphibians (anamniotes) is currently being re-evaluated in terms of evolution and several evidences have corroborated numerous traits shared by amphibians and amniotes, such as the organization of the basal ganglia and the amygdaloid complex. In the present study we have analysed the organization of forebrain afferent systems to the hypothalamus of the frog Rana perezi. In vivo and in vitro tract-tracing techniques with dextran amines and immunohistochemistry for localizing nitric oxide synthase (NOS) in a series of single or combined experiments were used as NOS labelling reveals hypothalamic afferents arising from the lateral amygdala and the combination allowed analysis of the relationship between fibers of different origins in the same section. The results showed a large segregation of afferents in the hypothalamic region depending on their site of origin in the forebrain. Four highly topographically organized prosencephalic tracts reaching the anuran hypothalamus were observed: (i) the medial forebrain bundle, from the medial pallium and septal complex; (ii) the caudal branch of the stria terminalis formed by fibers arising in the lateral and medial amygdala; (iii) part of the lateral forebrain bundle with fibers from the central amygdala and (iv) the dorsal thalamo-hypothalamic tract. Fibers coursing in each tract reach the hypothalamus and terminate in distinct fields. The resemblance in pattern of forebrain-hypothalamic organization between amphibians and amniotes suggests that this feature represents an important trait conserved in the evolution of all tetrapods and therefore essential for the hypothalamic function.

Afferent Pathways↗
PubMed1982

[3H]Imipramine is accumulated but not released from slices of the rabbit caudate and hypothalamus.

Slices of rabbit caudate and hypothalamus take up and accumulate [3H]imipramine. In superfused slices of both structures electrical stimulation or exposure to tyramine failed to release recently taken up [3H]imipramine. Depolarization by exposure to 30--60 mM-potassium caused only a small release of [3H]imipramine that was not concentration-dependent. The release of [3H]imipramine by high potassium was independent of the presence of calcium ions in the superfusion medium. These results contrasted with those obtained for the release of [3H]dopamine from the caudate and [3H]noradrenaline from the hypothalamus, where tyramine, electrical stimulation, and high potassium caused a significant release of the labeled neurotransmitters. The release of [3H]dopamine from the caudate and [3H]noradrenaline from the hypothalamus elicited by electrical stimulation or high potassium was entirely calcium-dependent. It is concluded that [3H]imipramine is taken up into the two brain regions and is accumulated in a nonvesicular site from which it is not released by calcium-dependent depolarizing stimuli.

Amphetamine↗
PubMed1984

Comparative characterization of glutamate decarboxylase in crude homogenates of oviduct, ovary, and hypothalamus.

Some biochemical characteristics of L-glutamate decarboxylase (GAD) were compared using crude homogenates of the rat oviduct, ovary, and hypothalamus. As estimated by the measurement of CO2 production, the specific activities of oviductal and ovarian GAD were about 10 and 3% of the hypothalamic value, respectively. Stoichiometric formation of gamma-aminobutyric acid (GABA) and CO2 from L-glutamate could be observed in oviduct and hypothalamus, while in ovarian homogenates the production of CO2 was more than nine times that of GABA. Hypothalamic and tubal GAD showed similar time course, temperature dependence, and pH dependence. The dependence on protein concentration and on exogenous cofactor supply was also similar in these two tissues. The kinetic constant for L-glutamate as a substrate was nearly the same in oviduct (1.30 mM) and hypothalamus (1.64 mM). The responsiveness of tubal and hypothalamic GAD to various inhibitors was also similar. The present findings indicate that the oviductal and the hypothalamic GAD may be identical, and they suggest a possible GABAergic innervation of the Fallopian tube.

Animals↗
PubMed1988

Effects of systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to mice on tyrosine hydroxylase, L-3,4-dihydroxyphenylalanine decarboxylase, dopamine beta-hydroxylase, and monoamine oxidase activities in the striatum and hypothalamus.

The effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (30 mg/kg subcutaneously per day for 8 days) to C57BL/6N mice were studied on tyrosine hydroxylase (TH), L-3,4-dihydroxyphenylalanine decarboxylase (DDC), and monoamine oxidase (MAO) activities in the striatum, and TH, DDC, dopamine-beta-hydroxylase (DBH), and MAO activities in the hypothalamus. Treatment with MPTP led to a large decrease in TH activity and a parallel decrease in DDC activity in the striatum, as compared with the saline controls. In contrast, MPTP administration did not cause a decrease of the activities of TH, DDC, and DBH in the hypothalamus. There was also no reduction in MAO activities of striatum and hypothalamus. These data indicate that MPTP administration to mice results in specific degeneration of the dopaminergic nigrostriatal pathway and that DDC in the mouse striatum may mainly be localized in the dopaminergic neurons with TH.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1989

tele-Methylhistamine levels and histamine turnover in nuclei of the rat hypothalamus and amygdala.

An HPLC method using fluorescence detection for the determination of tele-methylhistamine (t-MH) was improved to a sensitivity level which enabled the detection of 0.05 pmol of tissue t-MH. The t-MH contents and the histamine turnover rates in various nuclei of the rat hypothalamus and amygdala were subsequently measured. The histamine turnover rates were estimated from pargyline-induced t-MH accumulation. Both the t-MH levels and the histamine turnover rates were shown to be relatively high in the nuclei dorsomedialis and premammillaris ventralis of the hypothalamus, and also in the nucleus medialis of the amygdala. The steady-state t-MH levels in various nuclei of the hypothalamus and amygdala correlated well with the histamine turnover rates in these nuclei.

Amygdala↗
PubMed1991

The posttranslational processing of beta-endorphin in human hypothalamus.

beta-Endorphin is posttranslationally processed to six derivatives, which, although structurally similar, produce distinctly different biological effects. beta-Endorphin 1-31 is a potent opioid receptor agonist, but beta-endorphin 1-27 exhibits antagonist properties, and beta-endorphin 1-26 and the alpha-N-acetyl derivatives of all three peptides lack opioid receptor activity. In the present study, we identified the beta-endorphin peptides synthesized in human hypothalamus using cation exchange HPLC. First, we tested whether postmortem changes occur by storing rat hypothalami at 4 degrees C. This demonstrated that relative amounts of the six beta-endorphin forms did not change for up to 24 h, although total beta-endorphin immunoreactivity significantly declined after 6 h. HPLC analysis of human hypothalami revealed that beta-endorphin 1-31 was the principal form, constituting 58.4 +/- 5.4% of total immunoreactivity. Substantial amounts of beta-endorphin 1-27 (13.4 +/- 1.2%) and beta-endorphin 1-26 (13.1 +/- 1.6%) were also present, but alpha-N-acetylated forms were quantitatively minor, each comprising approximately 5% of total beta-endorphin. A similar processing pattern occurred in preoptic and suprachiasmatic areas of the hypothalamus. These results show that, despite differences in primary sequence, beta-endorphin is processed similarly in both rat and human hypothalamus. Opiate-active beta-endorphin 1-31 is the principal form in both species.

Adult↗
PubMed1993

Corticotropin-releasing factor stimulates catecholamine release in hypothalamus and prefrontal cortex in freely moving rats as assessed by microdialysis.

In vivo microdialysis was used to measure changes in extracellular concentrations of catecholamines and indoleamines in freely moving rats in response to administration of corticotropin-releasing factor (CRF). Dialysis probes were placed stereotaxically in either the medial hypothalamus or the medial prefrontal cortex. We used a repeated-measures design in which each rat received artificial CSF or one dose of CRF 3-4 h apart, and each subject was retested with the same treatments in the reverse order 5-7 days later. With the dialysis probe in the hypothalamus, intracerebroventricular administration of CRF (17 or 330 pmol) dose-dependently increased dialysate concentrations of norepinephrine (NE), dopamine (DA), and all their measurable catabolites except normetanephrine. The effects on NE were substantially greater than those on DA. Dialysate concentrations of serotonin could not be measured reliably, but those of its catabolite, 5-hydroxyindoleacetic acid, were also elevated. Concentrations of NE and DA were elevated within the first one or two (20 min) collection periods, with a peak response at approximately 1-2 h. Dialysate concentrations of catecholamines and metabolites normally returned to baseline within 3 h. Similar data were obtained with dialysis probes in the medial prefrontal cortex after intracerebroventricular administration of 17 or 167 pmol of CRF, except that the increases in DA exceeded those of NE in this region. Intraperitoneal administration of CRF (1 nmol) similarly elevated dialysate concentrations of NE, DA, 5-hydroxyindoleacetic acid, and all catecholamine catabolites except normetanephrine in both medial hypothalamus and medial prefrontal cortex. These results support earlier neurochemical data suggesting that CRF administered both centrally and peripherally stimulates the release of both DA and NE in the brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2006

Tumor necrosis factor-alpha activates signal transduction in hypothalamus and modulates the expression of pro-inflammatory proteins and orexigenic/anorexigenic neurotransmitters.

Tumor necrosis factor-alpha (TNF-alpha) is known to participate in the wastage syndrome that accompanies cancer and severe infectious diseases. More recently, a role for TNF-alpha in the pathogenesis of type 2 diabetes mellitus and obesity has been shown. Much of the regulatory action exerted by TNF-alpha upon the control of energy stores depends on its action on the hypothalamus. In this study, we show that TNF-alpha activates canonical pro-inflammatory signal transduction pathways in the hypothalamus of rats. These signaling events lead to the transcriptional activation of an early responsive gene and to the induction of expression of cytokines and a cytokine responsive protein such as interleukin-1beta, interleukin-6, interleukin-10 and suppressor of cytokine signalling-3, respectively. In addition, TNF-alpha induces the expression of neurotransmitters involved in the control of feeding and thermogenesis. Thus, TNF-alpha may act directly in the hypothalamus inducing a pro-inflammatory response and the modulation of expression of neurotransmitters involved in energy homeostasis.

Animals↗
PubMed2006

Anatomical distribution and biochemical characterization of the novel RFamide peptide 26RFa in the human hypothalamus and spinal cord.

26RFa is a novel RFamide peptide originally isolated in the amphibian brain. The 26RFa precursor has been subsequently characterized in various mammalian species but, until now, the anatomical distribution and the molecular forms of 26RFa produced in the CNS of mammals, in particular in human, are unknown. In the present study, we have investigated the localization and the biochemical characteristics of 26RFa-like immunoreactivity (LI) in two regions of the human CNS--the hypothalamus and the spinal cord. Immunohistochemical labeling using specific antibodies against human 26RFa and in situ hybridization histochemistry revealed that in the human hypothalamus 26RFa-expressing neurons are located in the paraventricular and ventromedial nuclei. In the spinal cord, 26RFa-expressing neurons were observed in the dorsal and lateral horns. Characterization of 26RFa-related peptides showed that two distinct molecular forms of 26RFa are present in the human hypothalamus and spinal cord, i.e. 26RFa and an N-terminally elongated form of 43 amino acids designated 43RFa. These data provide the first evidence that 26RFa and 43RFa are actually produced in the human CNS. The distribution of 26RF-LI suggests that 26RFa and/or 43RFa may modulate feeding, sexual behavior and transmission of nociceptive stimuli.

Aged↗
PubMed1957

Effects of reserpine on blood-pressure responses evoked from the hypothalamus.

Different areas of the hypothalamus were stimulated by a stereotaxic technique before and after reserpine in unanaesthetized cats. Reserpine in a dose of 1 mg./kg. body weight increased the threshold of stimulation of hypothalamic areas in cats giving an initial pressor response. It decreased the threshold of stimulation of areas of the hypothalamus in animals giving an initial depressor response. Reserpine thus appeared to affect the hypothalamus directly in two ways. It depressed the sympathetic centres in the diencephalon and facilitated the parasympathetic ones.

Animals↗
PubMed1970

Time course of the effects of 6-hydroxydopamine on catecholamine-containing neurones in rat hypothalamus and striatum.

1. The effects of intraventricular injection of 6-hydroxydopamine (6-OHDA) on tyrosine hydroxylase activity, uptake of (3)H-noradrenaline and endogenous catecholamine concentration in rat hypothalamus and striatum were investigated at various times after the injection of 6-OHDA.2. In the hypothalamus after the injection of 250 mug of 6-OHDA there was a rapid decrease in tyrosine hydroxylase activity, (3)H-noradrenaline uptake and noradrenaline content, which was essentially complete within 2 hours.3. In the striatum after this dose of 6-OHDA there was a much slower reduction in tyrosine hydroxylase activity and (3)H-noradrenaline uptake during the first 48 h after drug injection. For the first 24 h the dopamine concentration in this brain area was increased significantly above control values, but had fallen below control values by 48 hours.4. After the injection of a smaller dose of 6-OHDA (25 mug) the only detectable change in the striatum was a rapid increase in the dopamine concentration. In the hypothalamus this dose induced a rapid depletion of noradrenaline, not accompanied initially by any significant reduction in tyrosine hydroxylase activity.5. These results are consistent with the hypothesis that 6-OHDA causes a rapid degeneration of catecholamine-containing nerve terminals in the central nervous system (CNS). These degenerative changes, indicated by the loss of tyrosine hydroxylase and noradrenaline uptake sites, did not appear to be preceded by an initial displacement of endogenous catecholamines by 6-OHDA, except possibly at early times after the administration of small doses of the drug.

Animals↗
PubMed1982

Effect of stress and dexamethasone on immunoreactive beta-endorphin levels in rat hypothalamus and pineal.

In response to mild stress the levels of immunoreactive beta-endorphin in rat anterior pituitary, hypothalamus and pineal fell within 10 minutes from 210 to 129 pmol/lobe, 1.47 to 0.89 pmol/mg protein and 2.53 to 0.41 pmol/gland, respectively. No alterations were found to take place in beta-endorphin levels in posterior pituitary or plasma. Dexamethasone pretreatment given 18 h prior to stress resulted in significantly greater reduction of beta-endorphin levels in hypothalamus and pineal than stress alone--hypothalamic levels fell to 0.73 pmol/mg protein and pineal to 0.07 pmol/gland. Plasma beta-endorphin levels in dexamethasone pretreated stressed rats were significantly lower than in intact rats (42 fmol/ml vs. 98 fmol/ml). The almost complete disappearance of beta-endorphin from the pineal in response to stress and dexamethasone suggests that pineal does not itself synthesize the hormone but only utilizes and/or stores it. Gel filtration analysis of the beta-endorphin immunoreactivity in tissue extracts and plasma showed that anterior pituitary and plasma contain three immunoreactive components, eluting like beta-endorphin, beta-lipotropin and proopiocortin, whereas only beta-endorphin-like material was detected in posterior pituitary, hypothalamus and pineal.

Animals↗