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.

SourceResearch connectionFrom yearThrough year

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

At least 829 records · Page 46Linked to original sources

PubMed2002

Neurons expressing neuropeptide Y mRNA in the infundibular hypothalamus of Japanese quail are activated by fasting and co-express agouti-related protein mRNA.

The neural mechanisms involved in the compensatory hyperphagia exhibited by many vertebrate species after a fast are not fully understood but, in mammals, appear to involve nutritionally-sensitive neurons that co-express neuropeptide Y (NPY) and agouti-related protein (AGRP) in the infundibular hypothalamus. We investigated whether these neurons have been evolutionarily conserved in a non-mammalian vertebrate, the Japanese quail. Birds exhibited compensatory hyperphagia 1 h after return of food following a 24-h fast. We addressed a potential regulatory role for NPY, first, by using in situ hybridisation (ISH) to map NPY gene expression in the hypothalamus. This revealed a strong signal in the infundibular nucleus (IN). Secondly, we quantified NPY gene expression in 24-h fasted birds compared to ad libitum fed controls using two independent methods. In whole hypothalamus, measured by ribonuclease protection assay, NPY mRNA increased 1.5-fold in fasted birds. A similar, 1.7-fold, increase was observed specifically in the IN when analysed by ISH. No differences in NPY expression between fed and fasted birds were observed in other brain regions. To determine whether NPY neurons in the avian IN co-express AGRP, we cloned a fragment of the quail AGRP gene and used it to localise AGRP mRNA by ISH. The gene was expressed exclusively in the hypothalamus, specifically in the IN, where its distribution matched that of NPY. Double-label ISH revealed that the majority of NPY neurons in the IN co-express AGRP mRNA. Collectively, these data indicate that this cell type has been neuroanatomically and functionally conserved during vertebrate evolution.

Agouti-Related Protein↗

PubMed2000

Secretin, glucagon, gastric inhibitory polypeptide, parathyroid hormone, and related peptides in the regulation of the hypothalamus- pituitary-adrenal axis.

Secretin, glucagon, gastric inhibitory polypeptide (GIP), and parathyroid hormone (PTH) belong, together with vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase (AC)-activating polypeptide, to a family of peptides (the VIP-secretin-glucagon family), which also includes growth hormone-releasing hormone and exendins. All the members of this peptide family possess a remarkable amino-acid sequence homology, and bind to G-protein-coupled receptors, whose signaling mechanism primarily involves AC/protein kinase A and phospholipase C/protein kinase C cascades. VIP and pituitary AC-activating polypeptide play a role in the regulation of the hypothalamus-pituitary-adrenal (HPA) axis, and in this review we survey findings that also other members of the VIP-secretin-glucagon family may have the same function. Secretin and secretin receptors are expressed in the hypothalamus and pituitary gland, and secretin inhibits adrenocorticotropic hormone (ACTH) release. No evidence is available for the presence of secretin receptors in adrenal glands, but secretin selectively depresses the glucocorticoid response to ACTH of dispersed zona fasciculata-reticularis (ZF/R) cells. Glucagon and glucagon-like peptide-1 are contained in the hypothalamus, and all the components of the HPA axis are provided with glucagon and glucagons-like-1 receptors. These peptides exert a short-term inhibitory effect on stress-induced pituitary ACTH release and depress the ZF/R cell response to ACTH by inhibiting the AC/protein kinase A cascade; they also stimulate hypothalamic arginine-vasopressin release. GIP receptors are present in the ZF/R of the normal adrenals, and are particularly abundant in some types of adrenocortical adenomas and hyperplasias. GIP, through the activation of the AC/protein kinase A cascade, evokes a sizeable glucocorticoid secretagogue effect, leading to the identification of a food/GIP-dependent Cushing's syndrome. PTH and PTH-related protein are expressed in the hypothalamus and pituitary gland, and PTH and PTH-related protein receptors in all the components of the HPA axis. Both peptides enhance ACTH and arginine-vasopressin release, as well as stimulate aldosterone and glucocorticoid secretion of dispersed zona glomerulosa and ZF/R cells, respectively. The involvement of growth hormone-releasing hormone and exendins in the functional regulation of the HPA axis has not yet been extensively investigated.

Amino Acid Sequence↗

PubMed2000

Identification of branching paraventricular neurons of the hypothalamus that project to the rostroventrolateral medulla and spinal cord.

The paraventricular nucleus of the hypothalamus has efferent connections to autonomic nuclei known to ultimately regulate cardiovascular function. Studies have revealed projections to the sympathetic preganglionic neurons of the spinal cord and presympathetic motor neurons of the rostral ventrolateral medulla. This study set out to establish whether the same neurons in the paraventricular nucleus innervate both these regions. In rats the fluorescent neuroanatomical tracers FluoroGold, Fast Blue or Dextran tetramethyl rhodamine were injected into either the rostral ventrolateral medulla or T2 region of the spinal cord. After a suitable survival period (five to seven days) three populations of neurons could be identified in the paraventricular nucleus, double-labelled neurons and single-labelled neurons resulting from the injections into the spinal cord or injections into the rostral ventrolateral medulla. The neurons were of similar size regardless of the dye content. Most neurons were found in the parvocellular subdivision of the mid rostral paraventricular nucleus. The number of labelled neurons decreased in the caudal sections. This study provides an anatomical basis for three means of influence that the paraventricular nucleus can have on sympathetic activity; a hierarchical in series projection via the rostral ventrolateral medulla; a projection running in parallel with this but bypassing the rostroventrolateral medulla; and a branching population innervating neurons in both the rostral ventrolateral medulla and spinal cord. The paraventricular nucleus of the hypothalamus is an important brain area concerned with maintaining cardiovascular homeostasis. This anatomical study has not only provided confirmatory evidence that direct projections arising from the paraventricular hypothalamic nucleus do project to the rostral ventrolateral medulla and spinal cord, regions known to influence cardiovascular regulation. The study has identified a branching projection originating in the paraventricular nucleus of the hypothalamus that projects to both the rostral ventrolateral medulla and the spinal cord. Thus the paraventricular nucleus of the hypothalamus has three pathways in which to influence cardiovascular homeostasis.

Amidines↗

PubMed1997

Neurotoxicity, blood-brain barrier breakdown, demyelination and remyelination associated with NMDA-induced lesions of the rat lateral hypothalamus.

Excitotoxins have been widely used to make lesions in the brains of experimental animals because they have the ability to destroy neurones while sparing fibres of passage. Because loss of fibres of passage can confound the interpretation of lesion effects, this property is of considerable value. Recently, however, there have been reports indicating that excitotoxins acting at different sites within the rat CNS not only destroy neurones but also strip myelin from fibres and compromise the integrity of the blood-brain barrier. However, some reports also indicate that the myelin content of the lesioned area recovers. Excitotoxic lesions of the lateral hypothalamus have been shown to produce local demyelination. The present studies sought to investigate this effect further by (1) defining the time course of demyelination and possible remyelination after excitotoxic lesions of the lateral hypothalamus made with N-methyl-D-aspartate (NMDA); (2) establishing the relationships between neuronal loss, de- and remyelination after various doses of NMDA; and (3) examining the integrity of the blood-brain barrier using an immunohistochemical probe. Our data show that after injection of NMDA into the lateral hypothalamus there was neuronal loss, blood-brain barrier disruption (followed by recovery over approximately 12 days), triggering of reactive gliosis, invasion of the lesioned area by cells from outwith the CNS, demyelination over an area coexistent with but not exceeding the area of neuronal loss, and remyelination. Remyelination occurred over a period of 3 months following the production of the lesion and was associated initially with blood vessels. It occurred across the whole of the lesioned area, not by encroachment from the borders. All doses of NMDA that produced neuronal death also produced demyelination. These data confirm that excitotoxic lesions of the lateral hypothalamus demyelinate fibres, but show for the first time that remyelination occurs here. They are consistent with reports concerning excitotoxin actions at other CNS sites and indicate that de- and remyelination after excitotoxic lesions is a ubiquitous process. Consideration should be given to this when using excitotoxins to make fibre-sparing lesions.

Animals↗

PubMed1997

Association between pituitary adenylate cyclase-activating polypeptide and thyrotropin-releasing hormone in the rat hypothalamus.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is present in many regions of the hypothalamus including the paraventricular nucleus (PVN). In this study the anatomical relationship between PACAP- and thyrotropin-releasing hormone (TRH)-immunoreactive neuronal elements was investigated in the rat hypothalamus. Using a well-characterized mouse monoclonal antibody against PACAP and a rabbit polyclonal antiserum against TRH, we found numerous nerve fibers with PACAP-immunoreactivity (ir) closely apposed to TRH neurons in the PVN suggesting synaptic contacts. Electron microscopy confirmed the presence of synapses between PACAP-ir terminals and TRH-ir perikarya and various dendritic profiles as well as between PACAP-ir terminals and unlabeled perikarya and small- to medium-sized dendrites. Coexistence of the two peptides in perikarya of the PVN was limited to only a few neurons in the periventricular subdivision, but PACAP-ir and TRH-ir extensively coexisted in perikarya of the perifornical cell group, medial preoptic area, lateral hypothalamus and dorsomedial nucleus. The interactions between PACAP-containing neuronal processes and TRH neurons in the PVN raise the possibility that PACAP modulates the secretion of TRH destined for regulation of anterior pituitary TSH. The more general association between PACAP and TRH in other regions of the hypothalamus suggests a further role for PACAP as a cofactor in the function of TRH neurons.

Animals↗

PubMed1999

Role of the dorsomedial hypothalamus in mediating the response to benzodiazepines on trial 2 in the elevated plus-maze test of anxiety.

Trial 2 in the elevated plus-maze provides an animal model of specific phobia (fear of heights). On this trial, rats no longer respond to benzodiazepines. The present experiment examined the role of the dorsomedial hypothalamus in mediating insensitivity to chlordiazepoxide on trial 2. Rats received a 5 min exposure to the maze, undrugged. Forty-eight hours later, rats injected with control infusions into the dorsomedial hypothalamus showed the usual lack of response to chlordiazepoxide (5 mg/kg, i.p.). However, those receiving lidocaine injections (40 micrograms/microliter in a volume of 0.2 microliter) in the dorsomedial hypothalamus (producing functional inactivation), immediately before trial 2, responded with an anxiolytic response to chlordiazepoxide, characterised by an increased percentage of time on the open arms and by an increased number of entries into, and time spent on, the distal portions of the open arms. Since the lidocaine injections were without anxiolytic effects, our results suggest that this region of the hypothalamus regulates the functional state of benzodiazepine receptors in other brain regions.

Animals↗

PubMedDate not supplied

Occurrence of GH deficiency in adult patients who underwent neurosurgery in the hypothalamus-pituitary area for non-functioning tumour masses.

Hypothalamus-pituitary tumours and their treatments (neurosurgery and/or radiotherapy) are major causes of acquired hypopituitarism. Scientific and clinical evidences show the positive effect of GH replacement therapy in severe adult GH deficiency (GHD) pointed toward the need of diagnostic screening of conditions at high risk for GHD. We screened 152 adults (82 males, 70 females; age: 52.3+/-1.2 years, age-range: 20-80 years, BMI: 26.4+/-0.8 kg/m(2)) in order to disclose the presence of GHD after neurosurgery for hypothalamus-pituitary tumours. The whole group (studied at least 3 months after neurosurgery) included: 111 non-functioning pituitary adenomas and 41 peri-pituitary tumours (24 craniopharyngiomas, 7 meningiomas, 5 cysts, 2 chondrosarcomas, 1 colesteatoma, 1 germinoma and 1 hemangiopericitoma). In 14 patients who underwent both neurosurgery and radiotherapy due to a tumour remnant, the somatotroph function was evaluated again 6 months after the end of radiotherapy. GHD was assumed to be shown by GH peak <5 microg/L (severe <3 microg/L) after Insulin Tolerance Test (ITT) or <16.5 microg/L (severe <9 microg/L) after GH-releasing hormone+arginine test (GHRH+ARG) (3rd and 1st centile limits of normality, respectively), two widely accepted provocative tests. Before neurosurgery GHD was present in 97/152 (63.8%) and resulted severe in 66/152 (43.4%) patients. After neurosurgery GHD was present in 122/152 (80.2%) and severe in 106/152 (69.7%). While 26 patients developed severe GHD (GHD) as consequence of neurosurgery, only one patient who had been classified as GHD before neurosurgery showed normal GH response after surgery. After neurosurgery, 91.0% (81/89) of the pan-hypopituitaric patients showed severe GHD. Considering the 14 patients who underwent also radiotherapy after neurosurgery, 7/14 had GHD before neurosurgery while 12/14 became severe GHD after radiotherapy in a context of pan-hypopituitarism. IGF-I levels below the 3rd age-related normal limits were present in 39.0% of patients in whom severe GHD was showed by provocative tests. In conclusion, this study shows that the occurrence of acquired severe GHD is extremely common in adult patients bearing non-functioning tumour masses in the hypothalamus-pituitary area and further increases after neurosurgery. All patients bearing non-functioning hypothalamus-pituitary tumours should undergo evaluation of their somatotroph function before and after neurosurgery that represents a condition at obvious more than high risk for hypopituitarism.

Adenoma↗

PubMed2002

Angiotensin and calcium signaling in the pituitary and hypothalamus.

1) In the rat pituitary, angiotensin type 1B receptors (AT1B) are located in lactotrophs and corticotrophs. 2) Activation of AT1B receptors are coupled to Gq/11 (Guanine protein coupled receptor, or GPCR); they increase phospholipase beta C (PLC) activity resulting in inositol 1,4,5 triphosphate (InsP3) and diacylglycerol (DAG) formation. A biphasic increase in [Ca2+]i triggered by InsP3 and DAG ensues. 3) As many GPCRs, AT1B pituitary receptors rapidly desensitize. 4) This was observed in the generation of InsP3, the mobilization of intracellular Ca(2+), and in prolactin release. Both homologous and heterologous desensitization was evidenced. 5) Desensitization of the angiotensin II type 1 (AT1) receptor in the pituitary shares similarities and differences with endogenously expressed or transfected AT1 receptors in different cell types. 6) In the pituitary hyperplasia generated by chronic estrogen treatment there was desensitization or alteration in angiotensin II (Ang II) evoked intracellular Ca2+ increase, InsP3 generation, and prolactin release. This correlates with a downregulation of AT1 receptors. 7) In particular, in hyperplastic cells Ang II failed to evoke a transient acute peak in [Ca2+]i, which was replaced by a persistent plateau phase of [Ca2+]i increase. 8) Different calcium channels participate in Ang II induced [Ca2+]i increase in control and hyperplastic cells. While spike phase in control cells is dependent on intracellular stores sensitive to thapsigargin, in hyperplastic cells plateau increase is dependent on extracellular calcium influx. 9) Signal transduction of the AT1 pituitary receptor is greatly modified by hyperplasia, and it may be an important mechanism in the control of the hyperplastic process. 10) In the hypothalamus and brain stem there is a predominant expression of AT1A and AT2 mRNA. 11) Ang II acts at specific receptors located on neurons in the hypothalamus and brain stem to elicit alterations in blood pressure, fluid intake, and hormone secretion. 12) Calcium channels play important roles in the Ang II induced behavioral and endocrine responses. 13) Ang II, in physiological concentrations, can activate AT1 receptors to stimulate both Ca2+ release from intracellular stores and Ca2+ influx from the extracellular space to increase [Ca2+]i in polygonal and stellate astroglia of the hypothalamus and brain stem. 14) In primary cell culture of neurons from newborn rat hypothalamus and brain stem, it has also been determined that Ang II elicits an AT1 receptor mediated inhibition of delayed rectifier K(+) current and a stimulation of Ca2+ current. 15) In primary cell cultures derived from the subfornical organ or the organum vasculosum laminae terminalis of newborn rat pups, Ang II produced a pronounced desensitization of the [Ca2+]i response. 16) Hypothalamic and pituitary Ang II systems are involved in different functions, some of which are related. At both levels Ang II signals through [Ca2+]i in a characteristic way.

Angiotensin II↗

PubMed2004

Functional asymmetry of the frontal cortex and lateral hypothalamus of cats during an operant food-related conditioned reflex.

The extent of correlation and the latency of evoked potentials to sound, recorded bilaterally in the frontal cortex and lateral hypothalamus of cats, were studied at different stages of the acquisition of an operant food-related reflex and during sudden transfer to 30% food reinforcement. High correlation coefficients between the evoked responses of the cortex and hypothalamus with left-sided dominance were seen in conditions of high levels of food motivation at the beginning of each experiment and in conditions of the high-probability appearance of the acquired conditioned reflex throughout the rest of the experiment. Comparison of the peak latencies of the early positive (P55-80) components of evoked potentials on the right and left sides showed that shorter latent periods were seen in the cortex on the left side at all behavioral stages, while this occurred (on the left side) in the hypothalamus only when the conditioned reflex was unfixed, while after fixation of the reflex and provision of 30% reinforcement, shorter latent periods were seen on the right side. It is concluded that the high level of left-sided correlation of evoked potentials in the hypothalamus was associated with the motivational and motor components of purposive behavior and was not associated with the emotional tension of the animals provoked by the disruption of the food reinforcement stereotype.

Acoustic Stimulation↗

PubMed2000

Brain structures and mechanisms involved in the control of cortical activation and wakefulness, with emphasis on the posterior hypothalamus and histaminergic neurons.

Wakefulness is a functional brain state that allows the performance of several "high brain functions", such as diverse behavioural, cognitive and emotional activities. Present knowledge at the whole animal or cellular level suggests that the maintenance of the cerebral cortex in this highly complex state necessitates the convergent and divergent activity of an ascending network within a large reticular zone, extending from the medulla to the forebrain and involving four major subcortical structures (the thalamus, basal forebrain, posterior hypothalamus and brainstem monoaminergic nuclei), their integral interconnections and several neurotransmitters, such as glutamate, acetylcholine, histamine and noradrenaline. In this mini-review, the importance of the thalamus, basal forebrain and brainstem monoaminergic neurons in wake control is briefly summarized, before turning our attention to the posterior hypothalamus and histaminergic neurons, which have been far less studied. Classical and recent experimental data are summarized, supporting the hypothesis that (1) the posterior hypothalamus constitutes one of the brain ascending activating systems and plays an important role in waking; (2) this function is mediated, in part, by histaminergic neurons, which constitute one of the excitatory sources for cortical activation during waking; (3) the mechanisms of histaminergic arousal involve both the ascending and descending projections of histaminergic neurons and their interactions with diverse neuronal populations, such as neurons in the pre-optic area and cholinergic neurons; and (4) other widespread-projecting neurons in the posterior hypothalamus also contribute to the tonic cortical activation during wakefulness and/or paradoxical sleep.

Journal Article↗

PubMed1991

Stress and the endocrine hypothalamus-pituitary-testis system: a review.

Stressors generally induce a depression of the hypothalamus-pituitary-testis (HPT) system, mediated by the activated hypothalamus-pituitary-adrenocortical (HPA) system, resulting in a fall in plasma luteinising hormone (LH) and testosterone levels. Hypothalamic gonadotrophin-releasing hormone (GnRH) secretion may be suppressed by endogenous opioid peptides (EOP) and/or corticosteroids. The latter dramatically enhance the negative feedback effects of testosterone on both the hypothalamus and pituitary. Pituitary gonadotrophin secretion may be reduced by adrenocorticotrophic hormone or by EOP of hypothalamic or pituitary origin. Decreases in plasma concentrations of testosterone, independent of gonadotrophins, can be induced by corticosteroids. These hormones might reduce the number of Leydig-cell LH-receptors or occupation of LH-receptors. Testicular steroidogenesis may also be inhibited by pro-opiomelanocortin-derived (opioid) peptides secreted by the Leydig cells. There are some indications of increases in LH and testosterone during acute stress and, in dominant male animals, during the stress of social conflict. The latter finding indicates a difference in stress response between dominant and subordinate males. In subordinate males, decreased feedback sensitivity may allow hypersecretion throughout the HPA system. As a result, corticotrophin releasing hormone may induce the release of EOP from the hypothalamus, which inhibit the HPT axis. This inhibition may be enhanced by a corticosteroid-induced decrease in testosterone feedback.

Animals↗

PubMed2005

Fos-positive neurons are increased in the nucleus of the solitary tract and decreased in the ventromedial hypothalamus and amygdala by a high-protein diet in rats.

Transition from a normal- (NP) to a high-protein (HP) diet induces a rapid depression in food intake and a progressive but incomplete return to the initial intake during the succeeding days. The aim of this study was to determine which CNS regions are involved in the HP diet-induced satiety in rats. Brains were collected from 3 groups of adult rats after habituation to an NP diet (21 d), during the transition phase to a HP diet (2 d), or after habituation to the HP diet (21 d). Fos expression was measured in several brain areas that are involved in the control of food intake (solitary tract nucleus, anterior piriform cortex, lateral hypothalamus, arcuate nucleus, posterior para ventricular nucleus, medio ventral hypothalamus, dorso medial hypothalamus, amygdala, and accumbens nucleus). Changes occurred in the majority of these regions during the transition period from the NP diet to the HP diet. After habituation to the HP diet, significant changes in Fos expression were restricted to an increase in the nucleus of the solitary tract and a decrease in the ventromedial hypothalamus and the cortex of the amygdala. Considering the functional characteristics of these areas, the present results suggest that the vagus nerve conveys the information relative to the quantity of protein ingested, that hypothalamic sites regulate food intake and may alter sympathetic nervous system activity, and that higher brain functions such as memory processing by the limbic system or food reward system are involved in the HP diet-induced satiety in rats.

Adaptation, Physiological↗

PubMed2000

The distribution of the neurokinin B receptor in the human and rat hypothalamus.

The neurokinin B receptor (NK3) is an element of the hypothalamic neuronal circuitry regulating blood pressure in rats. The present study used immunohistochemistry to reveal the distribution of NK3 in the human hypothalamus. The strongest NK3-like immunoreactivity in the human hypothalamus was found in neurons of the paraventricular nucleus, specifically in the parvicellular and posterior paraventricular subnuclei. Another prominent population of NK3-positive cells in the human hypothalamus was found in the perifornical nucleus. The present study also showed two previously unreported populations of NK3-positive neurons in the rat periventricular nucleus and medial magnocellular paraventricular subnucleus. It is concluded that there is a large degree of similarity in the distribution of NK3 in the human and rat hypothalamus.

Adult↗

PubMed1990

Distribution of Galanin mRNA Containing Cells and Galanin Receptor Binding Sites in Human and Rat Hypothalamus.

The distribution of cells containing galanin mRNA and that of galanin receptor binding sites were investigated using in situ hybridization histochemistry and receptor autoradiography in male rat hypothalamus and in postmortem hypothalamic tissues from control human brains. Oligonucleotide probes labelled with 32P were used for hybridization experiments. The specificity of the hybridization signal was ascertained using several probes, competition assays and Northern blot analysis. High levels of hybridization were found in the paraventricular, supraoptic and arcuate nuclei of rat and human hypothalamus. Human intermediate nuclei and scattered cells of the posterior perifornical nucleus also contained galanin mRNA. Galanin mRNA was also found in the dorsomedial nucleus of the rat. The distribution of galanin receptor sites was investigated by receptor autoradiography using 125I-labelled porcine galanin. The specificity of the binding was assessed by competition with different neuropeptides. While galanin blocked the binding at nanomolar concentrations, the other neuropeptides examined were ineffective at 10-7 M concentrations. The highest densities of galanin binding sites were seen in the preoptic area, ventromedial and lateral nuclei, of rat and human hypothalamus. In contrast, very low densities of binding sites were observed in the paraventricular, supraoptic and arcuate nuclei. Our results show that the distribution of neurons expressing galanin is complementary to that of galanin receptors in the rat and human hypothalamus. This suggests that receptors for galanin are not located on the cell bodies of galaninergic neurons, but are probably presynaptic on or postsynaptic to the processes of these cells.

Journal Article↗

PubMed1988

Plasma osmolality predicts extracellular fluid catechol concentrations in the lateral hypothalamus.

The lateral hypothalamus has an important role in regulating food and water intake. We have investigated the endogenous release of monoamines from the lateral hypothalamus during manipulations of plasma osmolality and circulating volume. Adult male Sprague-Dawley rats implanted with carbon paste in vivo electrochemical (EC) electrodes in the lateral hypothalamus were placed on a 72-h water deprivation schedule. Although the carbon paste EC electrode has an intrinsically ambiguous signal in which changes in ascorbic acid may appear as changes in catechol concentrations, pharmacologic studies in lateral hypothalamus indicated that the electrode most likely measured norepinephrine and possibly epinephrine. On the test day, the EC electrodes were scanned with linear sweep voltammetry from -0.2 to +0.4 V at a rate of 5 mV/s. Semiderivative signal processing showed catechol and hydroxyindole peaks at +0.11 and +0.23 V, respectively. Baseline recordings were made prior to rats drinking distilled water, 10% sucrose, 5% dextrose, 0.30% NaCl, 0.90% NaCl, or 10% d-mannitol. To control for the act of drinking, other implanted dehydrated rats were intraperitoneally injected with 5% dextrose, 0.30% NaCl, or 0.90% NaCl. To dissociate the effects of osmolality and circulating volume on the EC response, hydrated rats implanted with EC electrodes were subcutaneously injected with 12% NaCl or intraperitoneally injected with 35% polyethylene glycol. Other rats subjected to water deprivation and osmotic challenges were decapitated and trunk blood was collected for measurements of plasma osmolality and hematocrit. Similar experiments were conducted using homozygous Brattleboro rats which lack arginine vasopressin (AVP) but which preserve normal plasma osmolality with prodigious drinking.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Lower urinary tract function in patients with pituitary adenoma compressing hypothalamus.

BACKGROUND: The micturition reflex is under the tonic influence of suprapontine structures including the anteromedial frontal cortex, basal ganglia, and hypothalamus. However, there have been few reports about the role of the hypothalamus on the lower urinary tract (LUT) function in humans. OBJECTIVE: To investigate LUT function in patients with pituitary adenomas. METHODS: Urodynamic studies were carried out in three patients with LUT symptoms who had pituitary adenomas extending upwards to the hypothalamus. RESULTS: All three male patients (age 28 to 62 years) developed LUT symptoms (urinary urgency and frequency (3); urinary incontinence (3); voiding difficulty and retention (2)) along with weight loss, psychiatric symptoms, unsteady gait, and/or visual disturbances. One had the syndrome of inappropriate secretion of antidiuretic hormone, but none had diabetes insipidus. Two had resection of the tumour and subsequent radiation therapy, but LUT dysfunction persisted. The third patient had partial resection of the tumour to ameliorate hydrocephalus. Urodynamic studies showed detrusor overactivity during the storage phase in all patients; during the voiding phase there was underactive detrusor in two and non-relaxing sphincter in one. CONCLUSIONS: Hypothalamic lesions can cause severe LUT dysfunction in both the storage and voiding phases of micturition. This may reflect the crucial role of the hypothalamus in regulating micturition in humans.

Adenoma↗

PubMed1995

Alterations in extracellular GABA in the ventral hypothalamus of rats in response to acute glucoprivation.

gamma-Aminobutyric acidergic (GABA) mechanisms in the ventral hypothalamus may be involved in counterregulatory responses to glucoprivic episodes. Microdialysis probes (1 mm) were placed into the ventromedial hypothalamus (VMH) or lateral hypothalamus (LHA) of male Sprague-Dawley rats 3.5 h before 2-deoxy-D-glucose (2-DG) administration (200 mg/kg i.v.). Probes were perfused (2 ml/min) with Ringer solution, and samples were collected every 10 min from 30 min before to 60 min after 2-DG. By 30 min after 2-DG, GABA concentration in VMH dialysate increased in a bimodal fashion to 204 +/- 36% (P < 0.01) of baseline, and GABA concentration in LHA dialysate decreased to 77 +/- 4% (P < 0.01) of baseline. The changes in dialysate GABA concentrations occurred concurrently with the animals eating and returned to baseline by 60 min. When animals were denied access to food after 2-DG, the decrease in LHA GABA was not apparent and VMH GABA remained approximately 15% above baseline at the end of the sample period. The results of the present study provide evidence that GABAergic systems in the ventral hypothalamus are responsive to alterations in glucose status.

Acute Disease↗

PubMed1992

Diurnal corticotropin-releasing hormone mRNA variation in the hypothalamus exhibits a rhythm distinct from that of plasma corticosterone.

The hypothalamopituitary-adrenal axis exhibits a diurnal rhythm as witnessed by the daily excursion of corticosterone in plasma. The rhythm appears to be mediated largely by the stimulation of CRH neurons in the paraventricular nucleus (PVN) of the hypothalamus. In the present study, we investigated the effects of circadian influence on CRH mRNA levels in the paraventricular hypothalamus. Animals were sacrificed through a 24-hour period to establish a detailed time course of CRH mRNA fluctuations. Levels of both type I and type II corticosterone receptor mRNAs were also measured in this area to see whether changes correlate with that of CRH mRNA. Plasma levels of ACTH were quantified as an index for CRH peptide secretion. The results indicate that changes in ACTH closely paralleled alterations in corticosterone levels with an increasing trend starting at 1 PM, suggesting that the diurnal secretory drive commences around this time. The CRH mRNA rhythm as determined by RNase protection assays appeared to change in an anticipatory fashion to these endocrine fluctuations, increasing during the light phase and reaching maximal levels just prior to dark (5-6 PM). An abrupt decrease of 30% in the CRH mRNA content was detected in the hypothalamus within 2 h after dark (8 PM) and coincided with the peak of plasma corticosterone levels. However, other periodic variations in the CRH mRNA content were not accompanied by changes in plasma corticosterone. Neither types of corticosterone receptor mRNAs showed any diurnal change suggesting that the expression of steroid receptors in the hypothalamus is not regulated by circadian influences. We conclude that CRH mRNA levels fluctuate diurnally but are inversely related to corticosterone levels only in the early evening.

Adrenocorticotropic Hormone↗