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PubMed2006

Evidence for the presence of a glucosensor in hypothalamus, hindbrain, and Brockmann bodies of rainbow trout.

The aim of this study was to evaluate the existence of a glucosensor in different regions of the brain and in the Brockmann bodies (BB) of the rainbow trout, Oncorhynchus mykiss. Five groups (n = 12) of trout were injected intraperitoneally with saline alone (control) or saline-containing bovine glucagon (100 mug/kg), bovine insulin (4 mg/kg), 2-deoxy-d-glucose (100 mg/kg), or d-glucose (500 mg/kg) to promote hyperglycemia (glucagon, d-glucose, 2-deoxy-d-glucose) or hypoglycemia (insulin). Six hours after injection, samples from four brain regions (hypothalamus, telencephalon, hindbrain, and midbrain) and the entire BB were taken. Our results demonstrate within the BB and both the hypothalamus and hindbrain a metabolic response different to that observed in other tissues (midbrain, telencephalon) but similar to that described in tissues known to be glucosensors in mammals. The metabolic responses of these areas to changes in plasma glycemia were characterized by parallel changes in GLUT-2 expression, hexokinase-IV, or glucokinase activity and expression, glycolytic potential, and levels of glycogen and glucose. These changes are similar to those reported in mammalian pancreatic beta-cells and glucose-excited (GE) neurons, two cell types containing glucosensors. This study provides evidence for the presence of glucosensors responsive to hyper- and hypoglycemia in rainbow trout BB, hypothalamus, and hindbrain.

Animals↗
PubMed2002

Subdiaphragmatic vagotomy fails to inhibit intravenous leptin-induced IL-1beta expression in the hypothalamus.

Leptin is known to be an important circulating signal for regulation of food intake and body weight. Recent evidence has suggested that leptin is involved in infection and inflammation. The afferent vagus nerve is known to be an important component for transmitting peripheral immune signals to the brain, such as interleukin (IL)-1beta expression in the brain, anorexia, and fever responses. In the present study, we investigated whether intravenous leptin-induced IL-1beta expression in the hypothalamus is mediated via afferent vagus nerve. IL-1beta transcripts in the hypothalamus were significantly increased on RT-PCR assessment 1 h after the administration of leptin (1 mg/kg iv) to mice. Subdiaphragmatic vagotomy did not significantly modify intravenous leptin-induced IL-1beta expression in the hypothalamus compared with that in sham-treated mice. These data suggest that circulating leptin directly acts in the brain independently of afferent vagus nerve input originating from the subdiaphragmatic organs.

Animals↗
PubMed2005

Studies of oxytocin and vasopressin gene expression in the rat hypothalamus using exon- and intron-specific probes.

To develop a comprehensive approach for the study of oxytocin (OT) and vasopressin (VP) gene expression in the rat hypothalamus, we first developed an intronic riboprobe to measure OT heteronuclear RNA (hnRNA) levels by in situ hybridization histochemistry (ISHH). Using this 84-bp riboprobe, directed against intron 2 of the OT gene, we demonstrate strong and specific signals in neurons confined to the supraoptic (SON) and paraventricular (PVN) nuclei of the rat hypothalamus. We used this new intronic OT probe, together with other well-established intronic and exonic OT and VP probes, to reevaluate OT and VP gene expression in the hypothalamus under two classical physiological conditions, acute osmotic stimulation, and lactation. We found that magnocellular neurons in 7- to 8-day lactating female rats exhibit increased OT but not VP hnRNA. Since VP mRNA is increased during lactation, this suggests that decreased VP mRNA degradation during lactation may be responsible for this change. In contrast, whereas there was the expected large increase in VP hnRNA after acute salt loading, there was no change in OT hnRNA, suggesting that acute hyperosmotic stimuli produce increased VP but not OT gene transcription. Hence, the use of both exon- and intron-specific probes, which distinguish the changes in hnRNA and mRNA levels, respectively, can provide insight into the relative roles of transcription and mRNA degradation processes in changes in gene expression evoked by physiological stimuli.

Animals↗
PubMed1980

Projections to the hypothalamus from buffer nerves and nucleus tractus solitarius in the cat.

In 18 cats anesthetized with chloralose, electrical activity of spontaneously active hypothalamic units was monitored for changes in firing frequency during electrical stimulation of carotid sinus (CSN) and aortic depressor (ADN) nerves and the nucleus tractus solitarius (NTS). Stimulation of the CSN altered the activity of 55% (381/691) of the tested. These responsive units were widely distributed in the ipsi- and contralateral hypothalamus. Of the units tested during stimulation of the ADN only 6% (17/274) changed their firing frequency. Responsive units were located only on the ipsilateral side and primarily in the paraventricular and supraoptic nuclei, Electrical stimulation of the NTS altered the firing frequency of all 84 hypothalamic units previously identified by stimulation of the CSN. NTS stimulation elicited responses that had a significantly shorter latency and followed significantly higher frequencies of stimulation when compared to stimulation of the CSN. These results demonstrate that the two buffer nerves have distinctly different central projections to the hypothalamus and suggest different functional roles for the ADN and CSN in homeostatic regulatory mechanisms mediated by the hypothalamus.

Animals↗
PubMed1991

GABAA and excitatory amino acid receptors in dorsomedial hypothalamus and heart rate in rats.

We have previously shown that microinjection of drugs that interfere with the function of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) into the hypothalamus produces cardiorespiratory and behavioral changes resembling those seen in emotional stress. The purpose of this study was to determine whether excitatory amino acids (EAAs) can produce a cardiovascular response similar to that caused by the GABAA receptor antagonist bicuculline methiodide (BMI) when microinjected at the same hypothalamic site in urethan-anesthetized rats and to clarify the precise locus of action of these agents. N-methyl-D-aspartic acid (NMDA, 0.68-6.8 pmol/50 nl) and kainic acid (KA, 0.47-4.7 pmol/50 nl) produced dose-related increases in heart rate and blood pressure when injected at sites in the dorsomedial hypothalamus reactive to BMI (20 pmol/50 nl). Higher doses of NMDA (68 pmol), however, failed to elicit consistent increases in heart rate and blood pressure when injected at these same sites. The effects of NMDA were selectively blocked by the NMDA receptor antagonist 2-amino-5-phosphonopentanoic acid, whereas the effects of KA were selectively blocked by the non-NMDA EAA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione. These results demonstrate that 1) blockade of inhibitory amino acid receptors or stimulation of EAA receptors in the dorsomedial nucleus of the hypothalamus produces tachycardic and pressor responses in urethan-anesthetized rats and 2) use of high doses of EAAs may be an unreliable method of evoking local neuronal excitation in certain regions of the central nervous system.

2-Amino-5-phosphonovalerate↗
PubMed1996

Transplantation of lean fetal hypothalamus restores hypothalamic function in Zucker obese rats.

Rats with lesions to the ventromedial hypothalamus (VMH) manifest obesity, hyperphagia, and hyperinsulinemia, and fetal VMH transplantation into the third cerebroventricle of VMH-lesioned rats reduces the development of obesity caused by the lesion. The aim of this study was to determine whether the hyperphagia, hyperlipidemia, and hyperinsulinemia of obsese Zucker rats could be corrected by the transplantation of lean fetal Zucker hypothalamic tissue into the third cerebral ventricle of Zucker obese rats. After the fetal hypothalamic transplant (obese-HY), the rate of weight gain was significantly diminished compared with the unoperated Zucker obese rats and the obese rats that received the transplantation of a similar amount of frontal cortical tissue from the same fetus (obese-FC). Food intake was significantly lower, and plasma triacylglycerol and insulin concentrations were also significantly reduced in the obese-HY rats compared with the obese and obese-FC rats. The weight of the adrenal glands, the plasma adrenocorticotropic hormone concentration, the liver weight, and the liver lipid content in obese-HY were significantly less than those observed in the obese and obese-FC animals. There were no significant differences between the obese and the obese-FC animals or between unoperated Zucker lean rats and lean rats transplanted with lean fetal hypothalamus in all the parameters we determined in this study. Neovascularization and normal cellular morphology of the transplanted fetal hypothalamic tissue suggest that the transplanted neural and glial cells were viable and physiologically functional. In conclusion, this study offers evidence suggesting that the hypothalamic-pituitary-adrenal function is defective in Zucker obese rats, resulting in excessive weight gain, hyperphagia, hyperlipidemia, and hyperinsulinemia. The hypothalamic dysfunction in the Zucker obese rats is corrected by the transplantation of lean fetal hypothalamus.

Adrenal Glands↗
PubMed2000

Lipopolysaccharide effects on neuronal activity in rat basal forebrain and hypothalamus during sleep and waking.

Peripheral administration of lipopolysaccharide (LPS) is associated with alterations in sleep and the electroencephalogram. To evaluate potential neuronal mechanisms for the somnogenic effects of LPS administration, we used unanesthetized rats to survey the firing patterns of neurons in various regions of rat basal forebrain (BF) and hypothalamus during spontaneous sleep and waking and during the epochs of sleep and waking that occurred after the intraperitoneal administration of LPS. In the brain regions studied, LPS administration was associated with altered firing rates in 39% of the neurons examined. A larger proportion of LPS-responsive units showed vigilance-related alterations in firing rates compared with nonresponsive units. Approximately equal proportions of LPS-responsive neurons showed increased and decreased firing rates after LPS administration, with some units in the lateral preoptic area of the hypothalamus showing particularly robust increases. These findings are consistent with other studies showing vigilance-related changes in neuronal activity in various regions of BF and hypothalamus and further demonstrate that peripheral LPS administration alters neuronal firing rates in these structures during both sleep and waking.

Animals↗
PubMed2001

Noradrenergic and GABAergic systems in the medial hypothalamus are activated during hypoglycemia.

Noradrenergic and GABAergic systems in the medial hypothalamus influence plasma glucose and may be activated during glucoprivation. Microdialysis probes were placed into the ventromedial nucleus (VMH), lateral hypothalamus (LHA), and paraventricular nucleus (PVH) of male Sprague-Dawley rats to monitor extracellular concentrations of norepinephrine (NE) and GABA. During systemic hypoglycemia, induced by insulin (1.0 U/kg), NE concentrations increased in the VMH (P < 0.05) and PVH (P = 0.06) in a bimodal fashion during the first 10 min and 20-30 min after insulin administration. In the VMH, GABA concentrations increased (P < 0.05) in a similar manner as NE. Extracellular NE concentrations in the LHA were slightly lower (P = 0.13), and GABA levels remained at baseline. The increases in NE and GABA in the VMH were absent during euglycemic clamp; however, NE in the PVH still increased, reflecting a direct response to hyperinsulinemia. On the basis of these data, we propose that the activity of noradrenergic afferents to the medial hypothalamus is increased during hypoglycemia and influences the activity of local GABAergic systems to activate appropriate physiological compensatory mechanisms.

Animals↗
PubMed1993

The rostral hypothalamus: an area for the integration of autonomic and sensory responsiveness.

1. An investigation has been made of the effects of chemical stimulation of neurons in the rostral hypothalamus on cardiovascular and respiratory parameters and on a nociceptive viscerosomatic reflex (reflex activity recorded from a lumbar spinal nerve in response to electrical stimulation of visceral afferent fibers in the splanchnic nerve) in alphaxalone/alphadolone-anesthetised rats. 2. Neurons were stimulated by microinjection of DL-homocysteic acid (DLH) at ventromedial forebrain sites between 2 mm caudal and 3 mm rostral to bregma. Any changes were monitored in viscerosomatic reflex activity and in the rate and depth of respiration, arterial blood pressure, heart rate, and hindlimb muscle blood flow. 3. Viscero-somatic reflex activity was depressed to varying degrees after injection of DLH at 20/96 sites and this was always accompanied by some form of cardiovascular change. At 8 sites inhibition of the reflex was accompanied by a cardiovascular response that included an initial pressor response (type I response) and at the other 12 sites there was an initial depressor response (type II response). Injection of DLH at a further 30 sites evoked a depressor response and no change in viscerosomatic reflex activity and at the remaining 45 sites there was no detectable change in any of the variables measured. 4. The degree of inhibition evoked from type I sites (mean 90%) was significantly greater (P < 0.001) than that evoked from type II sites (mean 58%). Type I responses were only evoked from an extremely localized region in the rostral anterior hypothalamus that corresponds to the lateral area of the anterior hypothalamus.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2000

Gene expression in hypothalamus and brown adipose tissue of mice divergently selected for heat loss.

Gene expression was evaluated in mice divergently selected for 16 generations for heat loss, measured by direct calorimetry. The high (MH) heat loss line has approximately 50% greater heat loss, approximately 35% less body fat, approximately 20% greater feed intake, and twofold greater activity levels than the low (ML) heat loss line. At 11 wk, inbred males (developed from MH and ML) were euthanized 3 h after dark for dissection of tissues and extraction of RNA. Differential display PCR (DD-PCR) was used to evaluate transcriptional differences between lines in hypothalamus and brown adipose tissue (BAT). Evaluation was replicated within and across lines, using family pools of mRNA. Two genes were confirmed by competitive RT-PCR and/or Northern analysis to have greater levels of mRNA present in ML relative to MH mice. In both hypothalamus and BAT, the ribosomal protein L3 (RPL3) gene was expressed at higher levels in ML, whereas an unknown expressed sequence tag (EST) was also found at higher levels in the hypothalamus of ML mice. These results implicate RPL3 in regulation of energy balance and extend the genetic dissection of response to selection to the transcriptional level.

Adipose Tissue, Brown↗
PubMed2002

Neuropeptide Y, but not agouti-related peptide or melanin-concentrating hormone, is a target peptide for orexin-A feeding actions in the rat hypothalamus.

We examined the effects of orexin A on the mRNA levels of neuropeptide Y, agouti-related peptide, melanin-concentrating hormone, prepro-orexin and orexin receptors in the rat hypothalamus. Adult male rats were treated centrally (i.c.v.) with a single dose of orexin A (3 nmol). After 2, 6 and 12 h, neuropeptide Y, agouti-related peptide, melanin-concentrating hormone, and prepro-orexin mRNA levels were measured by semiquantitative RT-PCR and in situ hybridization; orexin receptors mRNA content was quantified by semiquantitative RT-PCR. We found that orexin A increased neuropeptide Y expression in the arcuate nucleus of the rat hypothalamus. This stimulatory effect was transient, being observed 2 h after the treatment, and disappearing after longer periods (6 and 12 h). In contrast, no change was demonstrated in hypothalamic agouti-related peptide, melanin-concentrating hormone, prepro-orexin or orexin receptors mRNA levels at any time evaluated. Our results suggest that neuropeptide Y synthesized in the arcuate nucleus of the hypothalamus, but not agouti-related peptide and melanin-concentrating hormone pathways, is likely involved in orexin-induced feeding behavior, and raise the possibility that this functional linkage may also be involved in other actions mediated by orexins such as locomotor activity and sympathetic function.

Agouti-Related Protein↗
PubMed1998

In vitro secretion of gonadotropin-releasing hormone (GnRH) and [hydroxyproline9]GnRH from the rat hypothalamus exhibits a differential sensitivity to castration and second messengers.

The decapeptide [hydroxyproline9]GnRH (HypGnRH) has been characterized as an endogenous posttranslational product of the gonadotropin-releasing hormone (GnRH) precursor in a wide range of mammalian brains. Despite consistent biological effects, its secretion by the hypothalamus remains hypothetical. We report here in vitro secretion of HypGnRH and GnRH by the hypothalamus from intact and castrated male rats and provide evidence that they are differentially regulated. Both peptides were identified by two anti-GnRH antibodies of different specificities after separation under two high-performance liquid chromatography conditions. Calcium dependency of HypGnRH release was demonstrated under stimulation with KCl in the absence or presence of Ca2+, as well as with Bay K 8644, veratridine, methoxyverapamil, or tetrodotoxin. Activation of signaling pathways involving adenylate cyclase and protein kinases A and C (PKC) induced HypGnRH release. Expression of data as percentage of release over tissue stores revealed a two- to threefold higher release of HypGnRH than of GnRH under the different modes of stimulation used, except under PKC activation which triggered a comparable recruitment of both peptides. Castration selectively affected PKC-coupled GnRH secretion which showed a twofold lesser release than in intact rats, while the HypGnRH release was unaffected. We conclude that HypGnRH and GnRH are not secreted from the hypothalamus according to the same mechanisms.

Adenylyl Cyclases↗
PubMed2000

Ontogeny of immunoreactive prostaglandin endoperoxide synthase isoforms in ovine fetal pituitary, hypothalamus and brainstem.

Parturition is initiated in sheep by an increase in the activity of the fetal hypothalamus-pituitary-adrenal (HPA) axis. Prostaglandins, known to augment the activity of this endocrine axis, have long been proposed as involved in the initiation of paturition. We have previously demonstrated that endogenously produced prostanoids augment the activity of the HPA axis, and we have proposed that the increased production of prostanoids within the fetal brain or pituitary at the end of gestation might be involved in the initiation of parturition. An important regulatory step in the biosynthesis of prostanoids is the activity of prostaglandin endoperoxide synthase (PGHS). The present study was designed to test the hypothesis that the abundance of one or both isoforms of PGHS (PGHS-1 and PGHS-2) increase in brain and/or pituitary at the end of gestation. We used immunoblot analysis to measure the abundance of immunoreactive PGHS-1 and PGHS-2 in pituitary, hypothalamus and brainstem collected from fetuses of known gestational ages. We found that the abundance of PGHS-1 was weakly but significantly increased at the end of gestation in the pituitary and brainstem. The abundance of PGHS-2, on the other hand, increased exponentially in the pituitary and hypothalamus with highest concentrations found in term fetuses. We conclude that these enzymes are developmentally regulated in pituitary and in brain regions important for HPA axis control. We speculate that the increased enzyme's abundance results in increased prostanoid biosynthesis near term, and is a link in the chain of events which initiates parturition.

Animals↗
PubMed2001

Neonatal imprinting and regulation of estrogen receptor alpha and beta mRNA expression by estrogen in the pituitary and hypothalamus of the male rat.

In male rodents, complete reproductive function is critically dependent on adequate estrogen action at different levels of the hypothalamic-pituitary-testicular axis. However, administration of high doses of estrogen during the critical period of neonatal differentiation results in multiple defects in the reproductive axis that disrupt male fertility, the molecular mechanism(s) behind such a phenotype remaining poorly characterized. The aim of this study was twofold: (1) to characterize the effects of neonatal estrogenization upon the pattern of estrogen receptors ERalpha and ERbeta mRNA expression in the pituitary and hypothalamus of the male rat, and (2) to evaluate the ability of estrogen to acutely regulate pituitary and hypothalamic ERalpha and ERbeta mRNA expression in the male rat. To achieve the first goal, groups of male rats were treated on the first day of life with estradiol benzoate (EB; 500 microg/rat), and pituitary and hypothalamic expression of ERalpha and ERbeta mRNA levels were assayed by semiquantitative RT-PCR at different ages from the neonatal period until adulthood (days 1-75 of life). In addition, the mechanism(s) of altered pituitary expression of ERalpha and ERbeta messages in neonatally estrogenized rats was explored by comparison of the effects of neonatal treatment with estrogen or a potent gonadotropin-releasing hormone (GnRH) antagonist. For the second goal, the acute effects of a single dose of EB (12.5-25 microg/rat) on hypothalamic and pituitary ERalpha and ERbeta mRNA expression were assessed in prepubertal and adult male rats. Neonatal estrogenization permanently decreased pituitary ERalpha and ERbeta mRNA expression levels respective to control values at all ages studied. This pattern of response was similar to the short-term effects of neonatal blockade of endogenous GnRH actions. In contrast, neonatal exposure to estrogen transiently increased the hypothalamic expression levels of ERalpha and ERbeta messages. This effect was detected in neonatal (5-day-old), infantile (15-day-old) and prepubertal (30-day-old) rats, and it disappeared at puberty. In addition, estrogen was able to acutely regulate mRNA expression levels of its cognate receptor subtypes in the pituitary and hypothalamus of intact male rats. In adult (75-day-old) males, EB administration (25 microg/rat) induced a significant time-dependent decrease in pituitary ERalpha and ERbeta mRNA levels. In contrast hypothalamic expression of ERalpha and ERbeta messages was increased after acute exposure to EB (12.5 microg/rat) in prepubertal males (30 days old); yet differences in the time course of the response to estrogen were noticed between targets. In conclusion, our data indicate that estrogen is able to neonatally imprint and acutely regulate mRNA expression levels of ERalpha and ERbeta in the pituitary and hypothalamus of the male rat. Regulation of pituitary and hypothalamic ERalpha and ERbeta gene expression by the cognate ligand represents a novel mechanism whereby estrogen modulates its own biological actions upon different levels of the male reproductive axis throughout the life span.

Animals↗
PubMed2001

Lactation alters gamma-aminobutyric acid neuronal activity in the hypothalamus and cerebral cortex in the rat.

Gamma-aminobutyric acid (GABA) neurons terminating in the hypothalamus have been implicated in the neuroendocrine regulation of reproductive hormones, particularly luteinizing hormone (LH) and prolactin. The aim of this study was to examine whether GABAergic neuronal activity in the hypothalamus was modified during lactation, and whether any observed changes correlated with changes in secretion of these hormones. Animals were divided into three experimental groups: diestrous controls, lactating with pups present (with pups), and lactating with pups removed for 4 h (without pups). Animals were decapitated either without treatment, or 60 min after inhibition of GABA degradation by aminooxyacetic acid (AOAA) (100 mg/kg, i.p.). The rate of GABA accumulation in the tissue after AOAA is a measure of GABA turnover. GABA turnover was estimated in 13 microdissected brain regions, and serum prolactin and LH measured by radioimmunoassay. Suckling was associated with significantly increased prolactin and significantly decreased LH compared with diestrous rats. In lactating rats with pups, GABA turnover was significantly increased in the cingulate cortex compared with diestrous rats. GABA turnover was significantly increased in the ventrolateral preoptic nucleus of lactating rats with pups compared with diestrous rats or lactating rats without pups. There was significantly lower GABA turnover in the anterior hypothalamic area, ventromedial and dorsomedial hypothalamic nuclei in lactating rats without pups compared with diestrous rats. There were no significant changes in other brain regions examined. The results demonstrate that activity of GABAergic neurons in specific parts of the hypothalamus and cerebral cortex is altered during lactation.

Animals↗
PubMed2001

Role of gonadal steroids in the corticotropin-releasing hormone and proopiomelanocortin gene expression response to Delta(9)-tetrahydrocannabinol in the hypothalamus of the rat.

Chronic exposure to Delta(9)-tetrahydrocannabinol (Delta(9)-THC) increases corticotropin-releasing hormone (CRH) and proopiomelanocortin (POMC) gene expression in the rat hypothalamus. The levels of circulating gonadal steroids concurrently modulate both neuropeptides in male and female rats. However, it remains unknown whether gonadal steroids regulate Delta(9)-THC effects on CRH and POMC gene expression in the hypothalamus of male and female rats. To explore this hypothesis, experiments were conducted on intact, 2-week-gonadectomized, 1-week-gonadectomized, 1-week-dihydrotestosterone (DHT)- or estradiol-replaced male and female rats. One week after hormonal replacement, animals were treated with vehicle or Delta(9)-THC (5 mg/kg/day, i.p. for 7 days). Administration of Delta(9)-THC to intact male rats increased CRH gene expression. Castration abolished Delta(9)-THC effects of CRH gene expression in males but not in females. On the other hand, POMC mRNA levels were reduced as a result of castration, and DHT treatment did not prevent this decrease. Delta(9)-THC treatment similarly increases POMC gene expression of intact, orchidectomized and DHT-replaced males. In females, ovariectomy decreased CRH gene expression. Delta(9)-THC administration increased CRH gene expression to the same extent in castrated and estradiol-replaced rats. On the other hand, POMC gene expression was increased by ovariectomy, and Delta(9)-THC administration did only increase POMC transcript levels in the estradiol-replaced group. These data show that gonadal steroids differentially regulate the effects of Delta(9)-THC on both CRH and POMC gene expression in the hypothalamus of male and female rats, suggesting gender differences in the reaction to cannabinoids.

Animals↗
PubMed2002

Effects of single and repeated restraint stresses on the expression of beta(1)-adrenoceptor mRNA in the rat hypothalamus and midbrain.

We examined the effects of single and repeated restraint stresses on the expression of beta(1)-adrenoceptor mRNA in the rat midbrain and hypothalamus using reverse transcriptase-polymerase chain reaction (RT-PCR). After the rats had been restrained for 4 h (single stress), or for 4 h per day during 2 or 3 consecutive days, the hypothalamus and midbrain were removed immediately and beta(1)-adrenoceptor mRNA levels in these regions were determined by RT-PCR. Single stress significantly decreased the mRNA level in the hypothalamus, but the mRNA level was near control levels after 2 and 3 days of stress. In the midbrain, single stress had no effect on the mRNA level, but 2 days of stress significantly increased it.

Animals↗
PubMed2003

Estradiol control of expression and levels of estradiol-binding proteins in the medial preoptic area, medial hypothalamus and pituitary.

The brains of mammals have at least three estradiol-binding proteins: estradiol receptor-alpha (ERalpha), ERbeta, and sex hormone-binding globulin (SHBG). In this study we compare the effects of estradiol treatment on the expression of mRNA for these three estradiol-binding proteins in two reproductively important brain areas, the medial preoptic area-anterior hypothalamus (MPOA-AH) and medial hypothalamus (MH) as well as in the hippocampus in ovariectomized rats, using the reverse transcriptase-polymerase chain reaction (RT-PCR). We also used surface-enhanced laser desorption ionization time of flight (SELDI-TOF) mass spectrometry (MS) to analyze the effects of estradiol in ovariectomized rats on SHBG levels in the MPOA-MH as well as the neurohypophysis. In vivo estradiol treatment in ovariectomized rats eliminated or significantly reduced expression of all three estradiol-binding proteins in both the MPOA-AH and MH. This change in ERalpha, ERbeta, and SHBG expression did not occur in the hippocampus. Both Northern blot and DNA sequence analysis confirmed the results of the RT-PCR for SHBG. SELDI-TOF MS analysis demonstrated that in vivo estradiol treatments resulted in dramatically decreased levels of SHBG in the hypothalamus and that a reduction in SHBG mRNA by estradiol treatment also resulted in a reduction in SHBG protein levels. Estradiol treatment also eliminated detectable SHBG from the neurohypophysis, suggesting that estradiol controls SHBG levels in this release site. That in vivo estradiol treatments had the same inhibitory effects on mRNA levels for SHBG and both ERs suggests similar translational control mechanisms for all three steroid-binding proteins in the brain. That estradiol treatments also reduced pituitary SHBG suggests that such treatment releases SHBG from the neurohypophysis.

Animals↗