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PubMed2000

The murine Otp homeobox gene plays an essential role in the specification of neuronal cell lineages in the developing hypothalamus.

Hypothalamic nuclei, including the anterior periventricular (aPV), paraventricular (PVN), and supraoptic (SON) nuclei strongly express the homeobox gene Orthopedia (Otp) during embryogenesis. Targeted inactivation of Otp in the mouse results in the loss of these nuclei in the homozygous null neonates. The Otp null hypothalamus fails to secrete neuropeptides somatostatin, arginine vasopressin, oxytocin, corticotropin-releasing hormone, and thyrotropin-releasing hormone in an appropriate spatial and temporal fashion, and leads to the death of Otp null pups shortly after birth. Failure to produce these neuropeptide hormones is evident prior to E15.5, indicating a failure in terminal differentiation of the aPV/PVN/SON neurons. Absence of elevated apoptotic activity, but reduced cell proliferation together with the ectopic activation of Six3 expression in the presumptive PVN, indicates a critical role for Otp in terminal differentiation and maturation of these neuroendocrine cell lineages. Otp employs distinct regulatory mechanisms to modulate the expression of specific molecular markers in the developing hypothalamus. At early embryonic stages, expression of Sim2 is immediately downregulated as a result of the absence of Otp, indicating a potential role for Otp as an upstream regulator of Sim2. In contrast, the regulation of Brn4 which is also expressed in the SON and PVN is independent of Otp function. Hence no strong evidence links Otp and Brn4 in the same regulatory pathway. The involvement of Otp and Sim1 in specifying specific hypothalamic neurosecretory cell lineages is shown to operate via distinct signaling pathways that partially overlap with Brn2.

Animals↗
PubMed1993

Pituitary of "cobalt" variant of the rainbow trout separated from the hypothalamus lacks most pars intermedial and neurohypophysial tissue.

Adenohypophysial cell types and neurohypophysial tissues were investigated in the cobalt variant of the rainbow trout, which possesses an irregularly-shaped pituitary. The pituitary remnant was completely detached from the hypothalamus in all but one fish, in which a remnant was associated with the hypothalamus. Prolactin (PRL) and growth hormone (GH) cells were predominant cell types in all pituitary remnants, forming PRL and GH areas, respectively. There were fewer somatolactin (SL) and melanophore-stimulating hormone cells than in normal fish. There were few corticotropin cells in cobalt and normal trout. Although aldehyde-fuchsin positive cells were also present, positively-staining fibers were not detected in any of remnants examined. Plasma SL levels were much lower in cobalt than in normal trout. Plasma levels of GH and T3 were significantly lower in cobalt than in normal fish. Plasma levels of PRL, T4 and cortisol, plasma osmolality, ions (Na+, K+, Ca2+, and Mg2+), glucose, triglyceride, free fatty acids, and amino nitrogen concentrations were similar in the two groups. Cobalt variants thus lack hypophysial pars intermedia and neurohypophysial tissues. Various abnormalities of the cobalt variant, such as the cobalt blue body color and the fat deposition in the abdominal cavity, may be related to the absence of the pars intermedia.

Animals↗
PubMed1996

Changes in poly(A) tail length of arginine vasotocin messenger ribonucleic acid in the hypothalamus of water-deprived chickens.

The effects of water deprivation on the secretion of vasotocin (AVT) and expression of the AVT gene were studied in White Leghorn cockerels. Animals deprived of water for 4 days were compared with normally hydrated controls. Blood samples were obtained for measurements of plasma osmolality and AVT levels, and the hypothalamus was collected for extraction of total cellular RNA. A 519-bp AVT cDNA was prepared by reverse transcriptase-polymerase chain reaction and a 209-bp PstI/EcoRI restriction fragment from the 3' region of the fowl AVT cDNA was used as a probe for Northern blot analysis. Plasma osmolality and AVT levels in dehydrated birds were about 30 and 350% greater, respectively, than those in normally hydrated controls. The quantity of hypothalamic AVT mRNA was 2. 3-fold greater in water-deprived birds compared to controls. The size of the hypothalamic AVT transcript was about 100-bp longer in the water-deprived birds. As determined by RNase H treatment in the presence and absence of oligo(dT)12-18, the increase in mean size of the AVT mRNA in dehydrated animals was due to a longer poly(A) tract. Our results indicate that osmotic stress up-regulates expression of the AVT gene and increases the accumulation of AVT mRNA in the hypothalamus. This accumulation may, in part, be due to lengthening of the AVT mRNA poly(A) tail which is a general mechanism associated with stabilization of vertebrate mRNAs.

Animals↗
PubMed1998

Specific binding sites for [3H]Dexamethasone in the hypothalamus of juvenile rainbow trout, Oncorhynchus mykiss.

Indirect evidence suggests that glucocorticoid hormones may act through cellular receptors to play a neuromodulatory role in the teleost CNS. We now report our findings on the use of [3H]dexamethasone (DEX) to identify hypothalamic glucocorticoid receptors (GRs) in juvenile rainbow trout, Oncorhynchus mykiss. Hypothalamic cytosol was incubated with [3H]DEX under various experimental paradigms with incubations terminated by addition of dextran-coated charcoal; following immediate centrifugation, a sample of bound [3H]DEX (supernatant) was collected and assessed for 3 H content. [3H]DEX binding was tissue dependent between 0.5 and 2. 0 hypothalamus equivalents per tube (1.0 to 4.7 mg protein, respectively). Specific binding (BSP) increased with time for 1.5 h and remained relatively constant for an additional 2.5 h; the calculated association rate constant was 2.23 x 10(8) M-1 x min-1. Equilibrium BSP was dissociated by addition of a 5000 M excess cortisol with an accompaning t1/2 of 1.25 h and dissociation rate constant of 0.553 min-1. BSP was saturable with a calculated equilibrium Kd and BMAX of 1.22 nM and 296 fmol/mg protein, respectively. BSP was displaced under equilibrium conditions by the corticosteroids, but to a lesser extent by the mineralocorticoid, estrogen, and progestin. The rank order of potency for [3H]DEX displacement was DEX > cortisol >> corticosterone > m triamcinolone = 11-deoxycortisol >> aldosterone > progesterone >>> 17 beta-estradiol. These properties of specifically bound [3H]DEX indicate the presence of a GR, similar to the mammalian cytosolic GR, in the hypothalamus of juvenile rainbow trout.

Animals↗
PubMed1998

An immunohistochemical study of temperature-related changes in galanin and nitric oxide synthase immunoreactivity in the hypothalamus of the toad.

Galanin (GAL) and nitric oxide synthase (NOS) have been implicated in the control of thermogenesis in mammals. An experimental protocol was designed to determine whether or not the expression of these molecules in the hypothalamus of the toad could be related to environmental temperature changes. Exposure of the animals to low temperature increased the number and intensity of NOS-positive neurons in the magnocellular hypothalamic region, in contrast to a weak immunoreactivity observed in control animals kept in a natural environment at a spring-summer temperature (23-27 degrees C). Also a significantly higher number of GAL-immunoreactive (-IR) cells was observed in the preoptic area as compared to that observed in controls, while no difference in the intensity of GAL immunostaining intensity was detected. These results show a temperature-related expression of GAL and NOS in the hypothalamus and preoptic area of the toad. The results suggest a possible role of GAL and NOS in the regulation of hibernation in these animals.

Acclimatization↗
PubMed2000

Pituitary proopiomelanocortin-derived peptides and hypothalamus-pituitary-interrenal axis activity in gilthead sea bream (Sparus aurata) during prolonged crowding stress: differential regulation of adrenocorticotropin hormone and alpha-melanocyte-stimulating hormone release by corticotropin-releasing hormone and thyrotropin-releasing hormone.

Plasma levels of cortisol, growth hormone (GH), adrenocorticotropin hormone (ACTH), alpha-melanocyte-stimulating hormone (alpha-MSH), N-acetyl-beta-endorphin, in vitro ACTH-stimulated cortisol secretion, and in vitro corticotropin-releasing hormone (CRH)- and thyrotropin-releasing hormone (TRH)-stimulated ACTH and alpha-MSH secretion were investigated in gilthead sea bream exposed to high stocking density (30 kg m(-3)) for 23 days. Within 3 days after the onset of crowding, plasma levels of cortisol, ACTH, alpha-MSH, and N-acetyl-beta-endorphin were above control values. After 7 days, plasma parameters had returned to control levels, but at 23 days, cortisol, alpha-MSH, and N-acetyl-beta-endorphin levels were again elevated over controls, indicating a long-term activation of the melanotrope cells. In contrast, crowding stress elicited a prolonged reduction in plasma GH levels concomitant with the increased hypothalamus-pituitary-interrenal axis (HPI) activation. Crowding stress enhanced cortisol secretory activity of the unstimulated interrenal cells. However, interrenal tissue from crowded fish in vitro displayed an attenuated response to ACTH stimulation compared with tissue from control fish, indicating a desensitization of these cells to ACTH during crowding. The involvement of pituitary proopiomelanocortin-derived peptides in the HPI axis of sea bream is indicated by the observed modulation of the CRH and TRH responsiveness of the corticotropes and melanotropes in crowded fish. At day 1, when there were crowding-induced plasma increases in ACTH and alpha-MSH, there was an attenuated CRH-stimulated but not TRH-stimulated, ACTH release. However, at that time, CRH- and TRH-induced responses of alpha-MSH secretion, and the unstimulated secretory activity of the MSH cells, were enhanced in crowded sea bream. These data provide evidence for stimulatory roles of multiple hypothalamic (CRH and TRH) and pituitary (ACTH and alpha-MSH) peptides in the activation of the hypothalamus-pituitary-interrenal axis under crowding conditions in sea bream.

Adrenocorticotropic Hormone↗
PubMed1994

The development of astrocytes immunoreactive for glial fibrillary acidic protein in the mediobasal hypothalamus of hypogonadal mice.

Numbers of astrocytes immunoreactive for glial fibrillary acidic protein (GFAP) are markedly increased in the mediobasal hypothalamus (MBH) of adult hypogonadal (hpg) mice. The astrocytosis cannot be reversed by administration of gonadal steroids. To investigate whether the glial changes are established in the perinatal period, when crucial developments occur in rodent brain, we determined the distribution of GFAP-IR astrocytes in normal and hpg mouse brain from birth to adulthood. The period up to 3 weeks of age was characterized by the gradual disappearance of radial glia and the increase in mature astrocytes in some brain regions, for example hippocampus. However, there were no apparent differences in GFAP-IR elements between normal and hpg brains and very few astrocytes in the MBH. From age 1 month, increased numbers of GFAP-IR astrocytes were apparent in the hypothalamus in hpg mice and this difference was more obvious at 2 months. By 4 months of age the characteristic astrocytosis in the MBH had been attained and this did not change in older hpg mice. These observations provide no evidence for upregulation of the GFAP gene during the first 2 postnatal weeks when its transcription is highest and astrocytes are proliferating most rapidly. It is more likely that the astrocyte response in the MBH in hpg mice reflects permanent differences in steroid-induced neuronal connectivity, caused by the hypogonadism.

Animals↗
PubMed1999

Increased nitric oxide concentrations in posterior hypothalamus and central sympathetic function on nitrate tolerance following subcutaneous nitroglycerin.

The present study was to examine the distributions of nitric oxide (NO) in the brain regions and peripheral vessels following subcutaneously administered nitroglycerin (NTG) and determine the noradrenergic activity and the role of central sympathetic function in acute nitrate tolerance. Tolerance to NTG was produced by subcutaneous (sc) administration of 4.0 mg NTG as four separate hourly pulse injections of 1.0 mg each in male (5-8 months) Sprague-Dawley rats. Rats in sham-treated group received sc injections of saline. Rats were killed by sodium pentobarbital (150 mg/kg, ip) at 10 min after last sc injection. The brain, gracilis muscle, aorta, superior mesenteric artery, coronary artery, and pulmonary vessels were quickly removed. Concentrations of nitrite (NO2-), nitrate (NO3-), and total NO2- plus NO3- (NOx-) were quantified in the micropunches of the anterior hypothalamus, the posterior hypothalamus (PH), the nucleus tractus solitarius, the lateral reticular nucleus, and the vessels in a blinded fashion. The central actions of acute tolerance to NTG were also determined using blockades of sympathetic functions in conscious rats. Four separate hourly pulse sc injections of 1.0 mg NTG produced a marked shift of the dose-response curve for arterial pressure depression induced by intravenous injection of the challenge doses of NTG. The same doses of sc NTG caused increases in NOx- [92+/-16% (mean +/- SE)] and NO3- productions (77+/-15%) in the PH, but did not significantly change in other brain regions (n = 6). NOx- and NO3- productions were significantly enhanced in the superior mesenteric artery, aorta, coronary artery, and pulmonary vessels following sc NTG, but were not altered in gracilis muscle by the treatment. The tolerance responses to arterial pressure depression were attenuated by intravenous administration of either prazosin (300 microg/kg), an alpha1-adrenoceptor antagonist, or chlorisondamine (10 mg/kg), a sympathetic ganglion blockading agent (n = 5-6). The results suggest that acute NTG tolerance predominately increases NO production in the PH. NO production was also markedly enhanced in the large and middle vessels but not in small vessels during acute NTG tolerance. The arterial pressure tolerance to NTG was reversed by blockade of central sympathetic function. We conclude that NO formation is increased in the PH following systemically administered NTG and NO in the PH may facilitate central sympathetic functions which contribute to nitrate tolerance.

Animals↗
PubMed1991

Relationships between the hypothalamus and adipose tissue mass.

The brain, particularly certain nuclei of the hypothalamus and their neural connections, have a major influence on energy balance, through effects on both food intake and energy expenditure. As summarized in Table 1, there are indeed extensive interactions between the hypothalamus and adipose tissue, the predominate site of storage of chemical energy. Structural, and possibly functional, abnormalities of the neural structures facilitate the development of obesity. This review has described four components of the interactive system. Two of these components are still partly conjectural; while we have increasing experimental support, the hypothalamic-pituitary-adipose axis and the hypothalamic-efferent neural-cytoskeletal pathway are the subject of continuing intense investigation. More complete knowledge of the pathophysiology of obesity will, in turn, facilitate prevention and treatment of corpulence, as well as such frequent associations as non-insulin dependent diabetes mellitus.

Adipose Tissue↗
PubMed1985

Gliomas of visual pathways and hypothalamus in children--a preliminary report.

26 children with gliomas of the visual pathway and hypothalamus were seen during 5 years. 4 of them had intraorbital tumors, in 22 children tumors were localized in the chiasmal/hypothalamic regions. In 25 patients the tumors were surgically explored. All 4 intraorbital gliomas were radically removed using a transcranial approach. Exploration without biopsy was performed 7 times, exploration plus limited biopsy in 3 cases. In the remaining 11 operated children partial or subtotal removal of the tumor was possible. One of the 18 histologically verified tumors was an anaplastic glioma, the others were typical pilocytic astrocytomas. 12 children had hydrocephalus. 7 patients died, 19 are still alive. The operative mortality was 4 out of our 25 operated cases (16%). All of these patients had large tumors with posterior spread into the hypothalamus. In future, surgery in these children should be confined to exploration and limited biopsy followed by radiotherapy. We advocate exploration and biopsy in all chiasma/hypothalamic tumors. The growth potential of these tumors is individually variable. We recommend to follow-up all patients at 3 months' intervals by means of visual evoked potentials, visual acuity, fundoscopy and visual field testing. CT scans and X-rays of the optic canals should be performed once a year. Surgery should only be considered if clinical and/or neuroradiological progression has been documented.

Adolescent↗
PubMed1996

Nitric oxide influences the release of histamine and glutamate in the rat hypothalamus.

To investigate the influence of nitric oxide (NO) on the release of histamine and glutamate, the anterior hypothalamus of anaesthetized rats was superfused through a push-pull cannula either with artificial cerebrospinal fluid (CSF) or with various drugs dissolved in CSF. Hypothalamic superfusion with the NO-donating compounds linsidomine (200 mumol/l) or diethylamine-NO (DEANO, 100 mumol/l) led to a pronounced and sustained decrease in the histamine release rate, whereas the release rate of glutamate was enhanced. Superfusion with the inhibitor of NO synthase L-NG-nitro-L-arginine methyl ester (L-NAME, 200 mumol/l) increased the histamine release rate. The inhibitory effect of 200 mumol/l linsidomine was abolished by atropine (10 mumol/l). Superfusion with the glutamate receptor agonists glutamate (100 mumol/l) or N-methyl-D-aspartate (NMDA, 50 mumol/l) enhanced the histamine release rate. In the presence of linsidomine, the releasing effect of NMDA was not changed. These findings demonstrate that the release of histamine in the hypothalamus is diminished by endogenous NO. This effect of NO on histamine release seems to be due to enhanced release of acetylcholine from vicinal cholinergic neurons via stimulation of muscarinic acetylcholine receptors located presynaptically on histaminergic neurons. The NO-induced glutamate release seems to exert a subordinate stimulatory effect on histamine release. Finally, the inhibition of histamine release by NO is not due to blockade of NMDA receptors.

Animals↗
PubMed1991

In vivo modulation of the histamine release in the hypothalamus by adrenoreceptor agonists and antagonists.

The modulation of the histamine release from histaminergic neurons by noradrenergic neurons was investigated by the push-pull technique. The posterior hypothalamus of the conscious, freely moving rat was superfused with artificial CSF through a push-pull cannula and the release of endogenous histamine was determined in the superfusate. Hypothalamic superfusion with a potassium-rich CSF enhanced the release rate of histamine. Superfusion with the alpha 2-agonists noradrenaline or clonidine diminished the release rate of histamine. Moreover, clonidine abolished the potassium-induced increase in the histamine release. Superfusion with the alpha 2-antagonists yohimbine or idazoxan enhanced the release rate of histamine. It is concluded that noradrenaline released from noradrenergic neurons of the hypothalamus modulates the release of histamine from histaminergic neurons by stimulating alpha 2-adrenoreceptors located on histaminergic nerve terminals.

Adrenergic alpha-Agonists↗
PubMed1993

Pulsatile release of catecholamines in the hypothalamus of conscious rats.

To investigate the patterns of catecholamine release in the brain, the hypothalamus of conscious, freely moving rats was superfused through a push-pull cannula with artificial cerebrospinal fluid and the catecholamines dopamine, noradrenaline and adrenaline were determined in the superfusate radioenzymatically. Superfusate was continuously collected in time periods of 20 min for at least 20 h. Dopamine, noradrenaline and adrenaline release rates fluctuated according to an ultradian rhythm with a frequency of 1 cycle/92 min (dopamine and noradrenaline) or 99 min (adrenaline). Additionally, the three catecholamines were released according to an ultradian rhythm with the following frequencies: noradrenaline and adrenaline 1 cycle/12 h, dopamine 1 cycle/8 h. The release rates of dopamine and adrenaline were similar during light and dark periods, while the release rate of noradrenaline in the dark period was slightly lower than that during the light period. It is concluded that in the hypothalamus of the conscious rat the release rates of dopamine, noradrenaline and adrenaline fluctuate according to two ultradian rhythms with different frequencies.

Activity Cycles↗
PubMed1989

Selective local action of angiotensin II on dopaminergic neurons in the rat hypothalamus in vivo.

Microdialysis was used to investigate whether angiotensin II modulates the basal and K+-induced release of endogenous noradrenaline, dopamine and their metabolites 3,4-dihydroxyphenylglycol (DOPEG) and 3,4-dihydroxyphenylacetic acid (DOPAC) from the anterior hypothalamus of the anaesthetized rat. The release of the amines was stimulated twice (ST1 and ST2) with either 50 mmol/l or 100 mmol/l K+. The release of each amine induced by K+ was reproducible and concentration-dependent. Angiotensin II when present in the perfusion fluid after ST1 at a concentration of 0.1 and 10 mumol/l (chosen after in vitro experiments had shown that the recovery of the peptide across the dialysis membrane was only 3.6%), had no significant effect on amine release. However, 10 mumol/l angiotensin II induced an immediate, significant increase in basal DOPAC outflow which reached a maximum of 89% in the 100 mmol/l K+ and 53% in the 50 mmol/l K+ experiments. No such effect was observed with DOPEG outflow. In a separate experimental series, addition of angiotensin II without a preceding K+ stimulation period did not significantly affect the outflow of the amines and metabolites. The results suggest that angiotensin II can selectively influence dopamine metabolism in the anterior hypothalamus in vivo but does not act locally to acutely facilitate the release of endogenous catecholamines from this brain area.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

GABAergic neurons in dissociated cultures of rat hypothalamus, septum, and midbrain.

Cultures of dissociated tissue blocks from 18 day-old rat embryos containing either septum plus anterior hypothalamus, retrochiasmatic hypothalamus, or midbrain, were maintained for 8-29 days in vitro. GABAergic neurons were visualized by incubation with (3H) gamma-aminobutyric acid followed by autoradiography and by immunocytochemistry using an antiserum against glutamic acid decarboxylase. Positive neurons were of variable shapes and sizes. Labeled neurons in the three cultured regions represented 3.4, 1.1 and 1.7%, respectively, of all neurons. Apart from a few exceptions, autoradiographic labeling and immunocytochemical staining coincided. Glial cells did not stain and showed very low grain densities. Radioactivity could be released from preloaded cultures upon depolarization by 50 mM potassium and 100 microM Veratridine. The demonstration of GABAergic neurons in cultures that are known to contain a variety of peptidergic neurons opens up the possibility of studying the interaction between the two classes of neurons in vitro.

Animals↗
PubMed1981

Immunocytochemical localization of neurotensin-containing neurons in the hypothalamus of the Japanese quail, Coturnix coturnix japonica.

The hypothalamus of Japanese quail, Coturnix coturnix japonica, has been studied by means of the peroxidase-antiperoxidase immunocytochemical method, with the use of antibodies to synthetic neurotensin (NT). A number of immunoreactive neuronal perikarya occur in the medial preoptic nucleus of the rostral hypothalamus and a few in the accessory part of paraventricular nucleus and dorsal portion of the infundibular nucleus. Some of them correspond to the parvocellular neurons previously identified tentatively as neurosecretory (Mikami et al. 1975, 1976). Large numbers of immunoreactive neuronal fibers are found in the preoptic area, which extend as a remarkable fiber tract from this area to the ventral septal area and to the subfornical organ. A few immunoreactive fibers also extend ventrocaudally to the infundibular nucleus and to the neural lobe.

Animals↗
PubMed1981

Hypophysiotropic neurons in the goldfish hypothalamus demonstrated by retrograde transport of horseradish peroxidase.

The horseradish-peroxidase (HRP) technique was used to visualize the cell bodies of axons projecting to the goldfish pituitary. Following intravenous injections of HRP, HRP reaction products were observed in axons of the rostral pars distalis, proximal pars distalis, neurointermediate lobe, pituitary stalk and in axons coursing from the pituitary into the hypothalamus. HRP-labelled cells in the brain were localized in two regions only - the nucleus preopticus (NPO) pars magnocellularis and pars parvocellularis, and the nucleus lateralis tuberis (NLT) of the hypothalamus. These observations suggest that the NPO and NLT are the source of the neurosecretory innervation of the goldfish pituitary.

Animals↗
PubMed1986

Light-microscopic immunocytochemical localization of growth hormone-releasing factor in the human hypothalamus.

The distribution of growth hormone-releasing factor (GRF)-like immunoreactivity in the human hypothalamus was studied by light-microscopic immunocytochemistry. With antibodies that we developed against synthetic human pancreatic GRF (hpGRF), we localized GRF immunoreactivity in neuronal cell bodies that were observed only in the infundibular (arcuate) nucleus. Immunostained nerve fibers were found in large numbers in the neurovascular zone of the median eminence, in the proximal portion of the pituitary stalk and in periventricular areas. These localizations are in agreement with those of studies recently performed in other species and strongly suggest that GRF can be released into the capillaries of the pituitary portal plexus to reach the anterior pituitary gland. The projections of GRF neurons in extra-infundibular regions suggest that GRF can also act as a neuromodulator or neurotransmitter in the hypothalamus.

Adult↗