Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HYPOTHALAMUS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources
PubMed1995

Gene expression of pituitary adenylate cyclase activating polypeptide (PACAP) in the rat hypothalamus.

Pituitary adenylate cyclase activating polypeptide (PACAP) isolated from ovine hypothalamus is considered to be a member of the vasoactive intestinal peptide/glucagon/secretin/growth hormone-releasing hormone family of peptides. Two forms of PACAP, PACAP38 and PACAP27, have been demonstrated in the rat hypothalamus. The PACAP precursor contains another peptide called PACAP-related peptide (PRP), but so far no information on this peptide in tissue exists. We have developed three radioimmunoassays specific for PACAP38, PACAP27 and PRP and demonstrate that all three preproPACAP peptides are expressed in the rat hypothalamus, the PACAP38/PACAP27 ratio being around 60 and the PACAP38/PRP ratio being around 10. HPLC analysis of hypothalamic extract showed that PACAP38 and PACAP27 are found in only one form corresponding to the respective synthetic peptides, whereas PRP eluted in two peaks, the predominant form corresponding to synthetic PRP1-29. The cellular distribution of PACAP38, PACAP27, and PRP and corresponding mRNA in the hypothalamus was determined with immunohistochemistry and in situ hybridization histochemistry. PACAP- and PRP-immunoreactive neuronal perikarya were observed in the medial parvocellular part of the paraventricular nucleus (PVN) in colchicine pretreated rats. Some cell bodies of magnocellular variety were found in the PVN. PACAP mRNA containing cells were observed in moderate numbers in the same parts of the paraventricular nucleus. PACAP- and PRP immunoreactive fibres and varicosities were distributed in the PVN and in the periventricular nucleus. These data show that PACAP38, PACAP27 and PRP are expressed in the parvocellular part of the PVN, implying roles as hypothalamic regulatory peptides.

Animals↗
PubMed1995

Temporal regulation by estrogen of beta-preprotachykinin mRNA expression in the rat ventromedial nucleus of the hypothalamus.

In the rat, reproduction and sexual behavior are controlled by the gonadal steroid regulation of synaptic interactions within the sexually dimorphic limbic-hypothalamic system. The effects of estrogen on the ventromedial nucleus of the hypothalamus, one nucleus within the circuit, are central to the modulation of this behavior. Involvement of the neuropeptide substance P, a member of the tachykinin family of neuropeptides, has been implicated in the regulation of both lordosis behavior and gonadotropin release. However, previous studies have provided conflicting evidence as to whether levels of substance P in the ventromedial nucleus of the hypothalamus are modulated by circulating estrogens. To study this question further, in situ hybridization histochemistry was used to examine levels of beta-preprotachykinin mRNA, which encodes substance P and other tachykinins, in the ventrolateral subdivision of the ventromedial hypothalamus at 10 consecutive timepoints over a 4 day period subsequent to an acute administration of estrogen. Following estrogen treatment, beta-preprotachykinin mRNA expression was increased in cells of the ventrolateral portion of the ventromedial nucleus of the hypothalamus which constitutively express beta-preprotachykinin mRNA; however, there were no statistically significant changes in the number of cells that express detectable levels of beta-preprotachykinin mRNA in the ventrolateral portion of the ventromedial nucleus. Estrogen treatment produced two peaks of beta-preprotachykinin mRNA expression, the first at 2 h and the second at 48 h after the injection of estrogen. These data indicate that estrogen has both rapid and prolonged effects on beta-preprotachykinin mRNA levels, suggesting that estrogen may affect different cellular mechanisms relevant to the induction of beta-preprotachykinin mRNA expression.

Animals↗
PubMedDate not supplied

In vitro, release of cholecystokinin from hypothalamus and frontal cortex of Sprague-Dawley, Zucker lean (Fa/-) and obese (fa/fa) rats.

Cholecystokinin (CCK) has been suggested as a putative satiety factor, whose site of action is in the hypothalamus. The genetically obese (fa/fa) Zucker rat has been proposed as a model of human obesity. Though hypothalamic tissue levels of CCK did not vary between the fa/fa rat and age-matched lean littermates (25.5 +/- 5.7 vs. 27.6 +/- 5.2 pmoles/g tissue) we sought to determine if the releasability of hypothalamic and cortical CCK was the same in lean and obese rats. The in vitro superfusion paradigm was used to study the release of CCK and substance P (sP) from hypothalamus, and CCK and vasoactive intestinal polypeptide (VIP) from frontal cortex. The potassium stimulated release of CCK from obese rat hypothalamic tissue was significantly higher than from lean rat hypothalamus (3.62 +/- 0.3 vs. 1.91 +/- 0.3 fmole equivalents CCK-8/mg tissue/10 min). Similarly, sP release was exaggerated in obese rats in a parallel fashion (5.56 +/- 0.44 vs. 2.761 +/- 0.46 fmoles/mg tissue/10 min). However, the potassium stimulated release of CCK and VIP from cortical tissue was the same in all three groups of rats. The obese Zucker rat thus, may have an anomalous release of CCK and sP from the hypothalamus, but not from the frontal cortex, an area not presumably associated with satiety.

Animals↗
PubMedDate not supplied

Regulation of histamine release in rat hypothalamus and hippocampus by presynaptic galanin receptors.

The effect of galanin, a peptide present in a subpopulation of histaminergic neurons emanating from the rat posterior hypothalamus, was investigated on K(+)-evoked [3H]histamine release in slices and synaptosomes from rat cerebral cortex, striatum, hippocampus and hypothalamus. Porcine galanin (0.3 microM) significantly inhibited histamine release induced by 25 mM K+ in slices from hypothalamus and hippocampus, but not from cerebral cortex and striatum, i.e., only in regions in which a colocalization of histamine and galanin has been described. The inhibitory effect of galanin was concentration dependent, with an EC50 value of 5.8 +/- 1.9 nM. The maximal inhibition was of 30-40% in hypothalamic and hippocampal slices depolarized with 25 mM K+. The galanin-induced inhibition observed in hypothalamic slices was not prevented in the presence of 0.6 microM tetrodotoxin and also occurred in hippocampal and hypothalamic synaptosomes, strongly suggesting the activation by galanin of presynaptic receptors located upon histaminergic nerve endings. The maximal inhibitory effect of galanin in slices or synaptosomes was lower than that previously reported for histamine acting at H3-autoreceptors, possibly suggesting that not all histaminergic axon terminals, even in the hypothalamus and hippocampus, are endowed with galanin receptors. It increased progressively in hypothalamic and hippocampal synaptosomes as the strength of the depolarizing stimulus was reduced. It is concluded that galanin modulates histamine release via presynaptic receptors, presumably autoreceptors located upon nerve terminals of a subpopulation of cerebral histaminergic neurons.

Animals↗
PubMedDate not supplied

The ovine hypothalamus and pituitary have markedly different distribution of C-type natriuretic peptide forms.

C-type natriuretic peptide (CNP) was measured in the hypothalamus and pituitary of four sheep by radioimmunoassay after extraction. The mean concentration of CNP in the hypothalamus was 1.01 +/- 0.08 pmol/g and 45.8 +/- 12.8 pmol/g in the pituitary. Analysis of these extracts by size exclusion HPLC showed the presence of two immunoreactive CNP components that cochromatographed with porcine CNP-53 and CNP-22 standards. Similar amounts of CNP-53- and CNP-22-like IR-CNP were present in the ovine hypothalamus (ratio 0.9:1), whereas in the pituitary, the bulk of the immunoreactive CNP was in the CNP-53-like form. These results show major differences in the distribution of IR-CNP forms between the hypothalamus and pituitary, which may reflect differences in CNP prohormone processing in these two tissues.

Animals↗
PubMed1995

Effect of hypophysectomy on pituitary adenylate cyclase activating polypeptide gene expression in the rat hypothalamus.

Pituitary adenylate cyclase activating polypeptide (PACAP) is a new member of the secretin/glucagon/vasoactive intestinal peptide (VIP) family. It stimulates adenylate cyclase in cultured rat pituitary cells, which have PACAP-specific receptors and expression of pituitary hormones. Therefore, PACAP is considered as a hypophysiotropic hormone. If so, there might be a feedback regulatory mechanism between pituitary hormones and hypothalamic PACAP. In the present study, we used nuclear run-on and RNase protection assays to examine whether transcription of the PACAP gene in the rat hypothalamus would change after hypophysectomy. PACAP levels in the hypothalamus were also determined by radioimmunoassay. The transcriptional rate of the PACAP gene and PACAP mRNA content decreased 1 and 2 weeks after hypophysectomy. Radioimmunoassayable PACAP levels in the hypothalamus also decreased after hypophysectomy. These findings suggest that the reduced rate of PACAP gene transcription after hypophysectomy causes the decreased mRNA and peptide levels in the hypothalamus. Replacement with GH, PRL, T4, corticosterone, and testosterone significantly restored PACAP mRNA levels in hypophysectomized rats to those in control animals. The results suggest that feedback regulation takes place between pituitary hormones or pituitary-dependent factors and hypothalamic PACAP.

Animals↗
PubMed1992

Positron emission tomography study of the human hypothalamus during normal ageing and in ischemic and degenerative disorders.

Regional blood flow and oxygen metabolism were determined by positron emission tomography, using the steady state technique with 15O, in the hypothalamus and in the whole brain of fifty two normal persons and patients suffering from cerebral ischemia and degenerative dementia. During normal ageing regional blood flow and oxygen consumption appeared to increase slightly in the hypothalamus and to decrease in the whole brain in 24 persons. In the young age group the hypothalamus was more protected against ischemia than in the elderly group. In the aged group with cerebral ischemia and degenerative dementia regional blood flow and oxygen consumption were decreased in the hypothalamus to the same extent as in the whole brain.

Adult↗
PubMed1983

Autoradiographic localization of estradiol- and progesterone-concentrating neurons in the isolated rhesus monkey hypothalamus.

Progesterone- and estradiol-concentrating neurons were autoradiographically localized in the in situ, vascularly isolated, rhesus monkey hypothalamus. Estradiol-concentrating neurons were dispersed throughout the hypothalamus, their density being greatest in the medial preoptic (MPOA) and medial basal hypothalamic nuclei (viz. dorsomedial, ventromedial (VMH) and infundibular nuclei). In contrast, progesterone-concentrating neurons were less densely localized in the medial preoptic, ventromedial (medial division) and infundibular nuclei. There was a virtual absence of progestin-concentrating cells in the anterior and posterior hypothalamic zones. This localization of cells was not attributed to the perfusion pattern of the isolated hypothalamus since a complete distribution of injected microspheres was found throughout the hypothalamus. The results of these studies indicate that a possible division between estradiol- and progesterone-concentrating neurons exists within the MPOA-medial basal hypothalamic nuclei of the rhesus monkey.

Animals↗
PubMed1990

Neurokinin A in the hypothalamus and anterior pituitary during the estrous cycle in the golden hamster.

The fluctuations in the neurokinin A concentrations in the hypothalamus and anterior pituitary of female golden hamsters were studied in the different stages of the estrous cycle, and they were correlated with the changes in serum estradiol levels. Neurokinin A levels in the hypothalamus were lowest at day 4 of the cycle (proestrus), when serum estradiol levels were highest. Neurokinin A levels in the hypothalamus of hamsters in day 1 (estrus), day 2 (diestrus I), and day 3 (diestrus II) were not significantly different from each other. In the anterior pituitary, the highest neurokinin A concentrations were found during day 1 of the cycle (estrus), the levels in day 2 (diestrus I), day 3 (diestrus II), and day 4 (proestrus) were significantly lower than at estrus, again showing the lowest levels during proestrus, when estradiol levels were maximal. These results show that neurokinin A levels in the hypothalamus and anterior pituitary of the female hamster undergo significant changes during the estrous cycle.

Animals↗
PubMed1991

Effects of morphine administration on catecholamine levels in rat brain; specific reduction of epinephrine concentration in hypothalamus.

The effects of morphine administration on concentrations of epinephrine, norepinephrine and dopamine were examined in the rat brain. Morphine injection reduced the epinephrine level only in the hypothalamus, while the norepinephrine level was reduced in the hypothalamus, medulla, and locus coeruleus. The dopamine concentration was elevated in all regions examined. These changes were blocked by administration of naloxone. Repeated injection of morphine for 14 days did not affect any catecholamine level. In naloxone-induced withdrawal, epinephrine was most markedly depleted in hypothalamus. These observations suggest that the epinephrine level in hypothalamus is affected by morphine acting on opioid receptors.

Animals↗
PubMed1993

Noradrenergic-GABAergic interaction in anterior hypothalamus from normotensive and sinoaortic denervated rats.

1. GABA content is decreased in anterior hypothalamus and medulla oblongata of hypertensive rats by sinoaortic denervation (SAD) when compared to control animals which underwent a sham-operation (sham). 2. Lesion of noradrenergic pathways by 6-hydroxydopamine (6-OHDA), intracerebroventricularly administered, induced depletion of noradrenergic content in frontal cortex, anterior and posterior hypothalamus in both SAD and sham-operated rats. 3. As a consequence of this noradrenergic depletion there was an increase of GABA content in anterior hypothalamus only, from sham- and SAD-operated animals, without changes in other areas. 4. There is a noradrenergic-GABAergic interaction in the anterior hypothalamus of normotensive rats which is not impaired in hypertensive rats by sinoaortic denervation.

Animals↗
PubMed1984

Neurotensin perfusion of rat hypothalamus: dissociation of dopamine release from body temperature change.

To determine whether endogenous dopamine is involved in the impairment of body temperature induced by neurotensin, the local activity of [14C]dopamine in the hypothalamus of the unanesthetized rat was examined. A push-pull guide tube was implanted permanently above an intended site of perfusion within the anterior hypothalamic, pre-optic area or other region of the diencephalon. After the endogenous stores of dopamine at a specific site were labelled by microinjection of 0.02-0.05 muCi of [14C]dopamine, an artificial cerebrospinal fluid was perfused at the site at a rate of 20 microliter/min and at successive 5 min intervals. Perfusion of neurotensin in concentrations of 0.05 or 0.1 microgram/microliter in the dorsomedial hypothalamus, lateral hypothalamus, arcuate nucleus or diagonal band of Broca evoked a calcium-dependent efflux of [14C]dopamine. The release of dopamine induced by neurotensin was functionally specific since it was: (1) not mimicked by the relatively inactive neurotensin analogue, [D-Arg9]neurotensin; (2) dependent on the morphological locus of the push-pull perfusion; and (3) not accompanied by an efflux of [3H]norepinephrine when the site was double-labelled. Although neurotensin perfused in the anterior hypothalamic, pre-optic area caused a consistent decline in temperature, in most cases the temperature change did not correlate with an enhanced release of dopamine. Moreover, the release of dopamine, but not the temperature change, was abolished when neurotensin was perfused in a calcium-free medium. These results show that it is unlikely that the thermolytic action of neurotensin, at least within the hypothalamus, is mediated by the presynaptic release of dopamine.

Animals↗
PubMed1985

Changes in the processing of beta-endorphin in the hypothalamus and pituitary gland of female rats during sexual maturation.

Puberty in the female rat is accompanied by a marked attenuation of the opioid inhibition of luteinizing hormone secretion. One factor which may contribute to this altered role is a change in the metabolism of opioid peptides during sexual maturation. beta-Endorphin undergoes a considerable degree of metabolism through both C-terminal proteolysis and N-acetylation, and these metabolites do not possess opioid activity. The processing of beta-endorphin in the hypothalamus and in the anterior and neurointermediate lobes of the pituitary gland in prepubertal and adult female rats was studied using gel filtration and high performance liquid chromatography coupled with radioimmunoassay. In the anterior lobe, high molecular weight precursors of beta-endorphin (pro-opiomelanocortin and beta-lipotropin) were present in prepubertal (28 days old) rats, but little authentic beta-endorphin was detected. In contrast, only beta-lipotropin and beta-endorphin were present in mature (70 days old) animals. Only beta-endorphin-sized peptides were present in the neurointermediate lobes of both prepubertal and adult rats. However, the proportion of N-acetylated metabolites was higher in sexually mature animals. In the hypothalamus, only beta-endorphin-sized peptides were present in both juvenile and adult animals. However, C-terminal proteolysis increased with age (no acetylated metabolites were detectable in this tissue). The proportion of the total beta-endorphin-like immunoreactivity attributable to beta-endorphin was lower in young adult (first dioestrus after vaginal opening) (55%) and mature (dioestrus, 61-64 days old) rats (56%) compared to prepubertal (30 days old) animals (75%) and the proportions of non-acetylated metabolites [beta-endorphin-(1-27) in young adults and beta-endorphin-(1-26) in adults] were increased concomitantly. These changes were correlated with a reduced luteinizing hormone response to the opiate antagonist naloxone in adult compared to prepubertal rats. beta-Endorphin is processed differently in the two lobes of the pituitary gland and in the hypothalamus and the degree of metabolism increases as the rat reaches sexual maturity. The increased metabolism of beta-endorphin in the hypothalamus, the site most likely to be involved in the control of luteinizing hormone secretion, results in a reduction in the relative proportion of the opioid active parent peptide. Thus, increased inactivation of beta-endorphin may contribute to the attenuation of the opioid inhibition of luteinizing hormone secretion observed during puberty.

Animals↗
PubMed1989

Ontogenesis of tyrosine hydroxylase-immunopositive structures in the rat hypothalamus. Fiber pathways and terminal fields.

The innervation of the hypothalamus and septal region by catecholaminergic fibers was studied in rats from the 12th fetal day until the 9th postnatal day. Catecholaminergic fibers were visualized with preembedding immunocytochemistry using antibodies to tyrosine hydroxylase. An intensification of diaminobenzidine product with silver and gold was additionally applied to increase the sensitivity and resolution power of the routine immunocytochemical technique. It has been demonstrated that, from the 13th fetal day, the hypothalamus and the septal region receive catecholaminergic fibers either belonging to the hypothalamic neurons or coming with the medial forebrain bundle from the outside of the hypothalamus. As the development of the hypothalamus proceeds, these fibers form the extensive networks within some neurosecretory centers either containing (the zona incerta, periventricular nucleus, etc.) or almost lacking (suprachiasmatic and paraventricular nuclei) the catecholaminergic neurons. In the former case, they terminate on the processes or perikarya of catecholaminergic neurons, while in the latter case their varicosities surround the immunonegative presumptive neurons in a basket-like manner. Moreover, from the 18th fetal day catecholaminergic fibers penetrate between the ependymal cells towards the 3rd ventricle and the primary capillary plexus of the hypophysial portal circulation, apparently providing the release of catecholamines to the cerebrospinal fluid and portal blood, respectively. The data obtained in this study are considered as the morphological basis for the involvement of the hypothalamic catecholamines in neuroendocrine regulations during ontogenesis.

Aging↗
PubMed1991

The histochemical demonstration of monoamine oxidase-containing neurons in the human hypothalamus.

Monoamine oxidase activity was revealed in a population of neurons, glial cells and some vessels in the post mortem human hypothalamus with monoamine oxidase histochemistry. The monoamine oxidase-containing neurons were observed in the caudal two-thirds of the basal hypothalamus, including the lateral hypothalamic area, tuberomammillary and posterior hypothalamic nucleus. The positive neurons were multipolar or fusiform in shape. The neuronal somata were medium to large in size, although the majority of the positive neurons were of a large type. The topographic localization of the monoamine oxidase-containing neurons in the human hypothalamus has been found to be more widespread than in the rat and cat hypothalamus, suggesting that the hypothalamic monoamine oxidase cell group is phylogenetically more highly organized in man compared with in the lower mammals.

Aged↗
PubMed1991

Regional distribution of somatostatin binding sites in the human hypothalamus: a quantitative autoradiographic study.

Using in vitro quantitative autoradiography and [125I]Tyr0-D-Trp8SRIF 14 as radioligand, we characterized the detailed distribution of somatostatin binding sites in human hypothalamus of both infants and adults. Guanosine triphosphate pretreatment, before incubation, allowed us to detect higher [125I]Tyr0-D-Trp8SRIF 14 binding site densities in hypothalamic structures such as preoptic and anterior hypothalamic areas and ventromedial and dorsomedial nuclei. In contrast, guanosine triphosphate was without effect in the other hypothalamic regions. The regional effects of guanosine triphosphate pretreatment were not different in infant and adult hypothalamus. Scatchard analysis showed that in a guanosine triphosphate-sensitive region (preoptic area) and a guanosine triphosphate-insensitive area (infundibular nucleus), [125I]Tyr0-D-Trp8SRIF 14 bound to a single class of binding sites. Affinities were similar in both regions, not modified by guanosine triphosphate pretreatment and not different in the adult (1.5 +/- 1.2 nM vs 3.2 +/- 2.1 nM for preoptic area and infundibular nucleus, respectively) and infant (0.9 +/- 0.5 nM vs 2.4 +/- 1.7 nM for preoptic area and infundibular nucleus). [125I]Tyr0-D-Trp8SRIF 14 binding sites were widely distributed in the anterior, mediobasal and posterior hypothalamus. Somatostatin 28 was twice as potent as somatostatin 14 to displace [125I]Tyr0-D-Trp8SRIF 14 binding in the preoptic area and infundibular nucleus. However, IC50s were 30 times lower in the preoptic area as compared with the infundibular nucleus. In adult as well as in infant, high densities were found mainly in the diagonal band of Broca, preoptic area and infundibular nucleus. Intermediate densities were localized in the anterior hypothalamic area, ventromedial, dorsomedial and lateral mammillary nuclei. The dorsal hypothalamic area, the paraventricular and medial mammillary nuclei displayed low but measurable densities. The only marked difference in the distribution of [125I]Tyr0-D-Trp8SRIF 14 binding sites in adult vs infant was observed in the medial and tuberal nuclei where the concentrations were seven-fold higher in adult hypothalamus.

Adult↗
PubMed1984

Vasopressin in reaggregated cell cultures of the developing hypothalamus.

A microsystem for rotation-mediated aggregate cell culture studies has been devised to examine vasopressin (VP) biosynthesis of developing rat hypothalamus. Trypsin-dispersed hypothalamic tissue was placed into 24 well tissue culture dishes and VP content of culture medium and cells was measured over time by a radioimmunoassay. Reaggregates formed within 4 hr when rotated at 70 rpm in a humid CO2 incubator. Nineteen days post coitus (dpc) hypothalamic reaggregates had 336 pg VP/10(6) cells while the medium showed 260 pg VP/ml after four days. Measurable VP was seen in fetal tissue after ten days while comparable amounts of VP were present in one day neonatal hypothalamus over this same period. Morphological examination of reaggregates indicated the presence of viable cells throughout the cell mass after ten days of culture. Co-cultivation studies with dispersed posterior pituitary indicated that reaggregates from one day neonate hypothalamus had significantly increased VP levels when co-cultured with one day neonatal posterior pituitary; however, this effect was not seen with 19 dpc co-cultures. These data demonstrate that development of neurosecretory activity of discrete regions of the hypothalamus can be examined early in vitro in a reaggregate cell culture system.

Animals↗
PubMed1986

Glucose regulates [3H](+)-amphetamine binding and Na+K+ ATPase activity in the hypothalamus: a proposed mechanism for the glucostatic control of feeding and satiety.

Binding sites for [3H](+)-amphetamine in the hypothalamus may mediate the anorectic actions of amphetamine and related phenylethylamines. To investigate further the role of these sites in the central control of appetite, the binding of [3H](+)-amphetamine to the hypothalamus and brainstem was measured following food deprivation and refeeding, the onset of genetic obesity, or the administration of 2-deoxy-D-glucose. Food deprivation for 24 to 72 hours reduced the Bmax for [3H](+)-amphetamine binding in the hypothalamus and brainstem but not in other brain areas or peripheral tissues. The decrease in hypothalamic and brainstem [3H](+)-amphetamine binding observed following food deprivation was time-dependent and rapidly reversed by brief refeeding with either rat chow or a 10% glucose solution. Moreover the changes in [3H](+)-amphetamine binding were highly correlated to corresponding alterations in blood glucose concentration. Furthermore, D-glucose, but not L-glucose increases the number of hypothalamic [3H](+)-amphetamine binding sites when administered in vivo or when added to hypothalamic slices in vitro. These data suggest that the [3H](+)-amphetamine binding site in the hypothalamus and (or) brainstem may be coupled to a central "glucostat."

Animals↗