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PubMed2001

Neonatal handling and the expression of immunoreactivity to tyrosine hydroxylase in the hypothalamus of adult male rats.

Neonatal handling has long-lasting effects on behavior and stress reactivity. The purpose of the present study was to investigate the effect of neonatal handling on the number of dopaminergic neurons in the hypothalamic nuclei of adult male rats as part of a series of studies that could explain the long-lasting effects of neonatal stimulation. Two groups of Wistar rats were studied: nonhandled (pups were left undisturbed, control) and handled (pups were handled for 1 min once a day during the first 10 days of life). At 75-80 days, the males were anesthetized and the brains were processed for immunohistochemistry. An anti-tyrosine hydroxylase antibody and the avidin-biotin-peroxidase method were used. Tyrosine hydroxylase-immunoreactive (TH-IR) neurons were counted bilaterally in the arcuate, paraventricular and periventricular nuclei of the hypothalamus in 30-microm sections at 120-microm intervals. Neonatal handling did not change the number of TH-IR neurons in the arcuate (1021 +/- 206, N = 6; 1020 +/- 150, N = 6; nonhandled and handled, respectively), paraventricular (584 +/- 85, N = 8; 682 +/- 62, N = 9) or periventricular (743 +/- 118, N = 7; 990 +/- 158, N = 7) nuclei of the hypothalamus. The absence of an effect on the number of dopaminergic cells in the hypothalamus indicates that the reduction in the amount of neurons induced by neonatal handling, as shown by other studies, is not a general phenomenon in the brain.

Animals↗
PubMed1978

Regulation of thyrotrophin secretion by negative feedback of tri-iodothyronine on the hypothalamus.

Bilateral injections of tri-iodothyronine (T3, 2 ng in 2 microliter artificial cerebrospinal fluid, CSF) were made into the hypothalami of 15 hypothyroid rhesus monkeys (Macaca mulatta) prepared with chronically implanted intrahypothalamic cannulae. In 29 out of 96 such injections, the concentration of thyrotrophin (TSH) in the plasma fell rapidly by more than 30% and returned to the basal value over the succeeding 48 h, in 13 experiments the fall was 20-30% and in the remaining 54 experiments the level of TSH was unaltered. With [125I]T3, the extent of diffusion of T3 through the hypothalamus in these experiments was shown to be very limited. The hypothalamic injection sites were subsequently identified histologically and it was found that in those experiments in which the level of TSH in the plasma had fallen, T3 had been injected into either the dorsomedial nucleus or the lateral hypothalamic area extending into the preoptic region. Injection of artificial CSF alone into these areas of the hypothalamus did not affect the concentration of TSH. Direct intrapituitary injections of T3 (4 ng) resulted in small and inconstant changes in the concentration of TSH in the plasma and injections of T3 (400 ng) into the third ventricle were without any effect. These experiments demonstrate that T3 can rapidly inhibit the secretion of TSH by a direct action upon defined parts of the hypothalamus.

Animals↗
PubMed1980

Alterations induced by clomiphene in the concentrations of oestrogen receptors in the uterus, pituitary gland and hypothalamus of female rats.

Alterations in the concentrations of oestrogen receptors in the uterus, pituitary gland and hypothalamus during the 2 weeks following a single administration of clomiphene citrate (Clomid) to immature, bilaterally ovariectomized rats were investigated. Examination of the uterine wet weight at 1, 7 and 14 days following a single injection of Clomid (100 micrograms, 250 micrograms or 10 mg) indicated significant time- and dose-related increments from a control value of 45 +/- 2 (S.E.M.) mg to a maximum of 123 +/- 3 mg (250 micrograms dose at 14 days). In contrast, a single injection of oestradiol led to a transient increase in the uterine weight on day 1 to 94 +/- 6 mg, but was without effect by days 7 and 14. Analysis of the uterine DNA content 7 and 14 days after treatment with Clomid revealed significant increments from control values of 390 +/- 10 micrograms to a high level of 558 +/- 9 micrograms (10 mg dose at 7 days). There was a transient retention of nuclear oestrogen receptors and rapid replenishment of cytoplasmic oestrogen receptors in less than 24 h in the uteri of animals treated with oestradiol (25 micrograms), but determinations of receptor content in Clomid-treated animals revealed prolonged retention of nuclear receptors and delayed replenishment of cytoplasmic receptors. The duration and extent of retention of nuclear receptors and depletion of cytoplasmic receptors after treatment with Clomid were found to be dose-dependent. Fourteen days after Clomid treatment, levels of oestrogen receptors in nuclei from the uterus were still raised in all treatment groups, whereas replenishment of cytoplasmic receptors was complete in animals treated with the lower doses (100 and 250 micrograms) of Clomid. A single injection of Clomid (250 micrograms) induced similar prolonged retention of nuclear receptors and delayed depletion of cytoplasmic receptors in pituitary tissue. In contrast, changes in the content of oestrogen receptors in the hypothalamus following Clomid treatment were minimal. The limited effect of Clomid on hypothalamic tissue may mean that the pituitary gland is a more important target for this compound than is the hypothalamus. The findings have confirmed earlier reports on the long-term uterotrophic effect of Clomid and have suggested that under these long-term, in-vivo conditions, Clomid acts in the uterus and pituitary gland as a long-acting oestrogen characterized by prolonged retention of oestrogen receptors in the nucleus and delayed, but otherwise effective, replenishment of the oestrogen receptors in the cytoplasm.

Animals↗
PubMed1983

Postnatal developmental pattern of thyrotrophin releasing hormone-degrading activity in rat plasma, hypothalamus and liver: role of tri-iodothyronine.

Thyrotrophin releasing hormone-degrading activity (TRH-DA) is present in plasma, hypothalamus, pituitary gland, liver and kidney of adults of several species. Each of these tissues contains more than one TRH-degrading enzyme but only one, pyroglutamate aminopeptidase, isolated from the blood, is a TRH-specific enzyme. The aim of this study was to describe the developmental pattern of TRH-DA in the plasma, hypothalamus and liver and the role of tri-iodothyronine (T3) in the development of TRH-DA in the rat. Based on the hypothesis that thyroid hormones stimulate plasma TRH-DA in adult rats, degradation of TRH was studied in hypo- or hyperthyroid rats induced by 6-n-propyl-2-thiouracil or T3 respectively. Tritiated TRH was incubated with plasma and homogenates of hypothalamus or liver. After separation of degradation products by thin-layer chromatography, the amount of degraded [3H]TRH (pmol/50 microliters plasma or homogenate) was taken as a comparative index of TRH-DA. Plasma TRH-DA was not detectable before day 9 while hypothalamic and hepatic TRH-DA was already active at birth. Furthermore, the maturation pattern of total TRH-DA was different in plasma compared with other tissues and T3 appeared to play a significant role in its development. The absence of plasma TRH-DA in the neonatal period, its special thyroid-dependent developmental pattern and the presence of a specific TRH-degrading enzyme in adult blood suggest a physiological regulatory role for this activity.

Animals↗
PubMed1985

Multiple forms of somatostatin-like immunoreactivity in the hypothalamus and amygdala of the rat: selective localization of somatostatin-28 in the median eminence.

The presence of multiple forms of somatostatin-like immunoreactivity (SSLI) in the rat hypothalamus was confirmed using a sensitive radioimmunoassay in conjunction with gel filtration chromatography and high performance liquid chromatography (HPLC). Gel filtration chromatography of hypothalamic extracts revealed the presence of four forms of SSLI with estimated molecular weights of 1500, 3000, 6000 and 10000. Analysis by HPLC indicated that the 1500 and 3000 mol. wt forms of SSLI corresponded respectively to somatostatin-14 (SS14) and somatostatin-28 (SS28) whereas the 6000 and 10000 mol. wt forms eluted together as a composite peak of high molecular weight somatostatin (HMW-SS). The proportions of SS14 (63%), SS28 (12%) and HMW-SS (25%) present in the hypothalamus were similar to those in the amygdala (59, 9 and 32% respectively). In contrast, the median eminence contained a greater proportion of SS28 than the other tissues: SS14, SS28 and HMW-SS were present in the proportions 40: 24: 26%. These results show that the rat median eminence differs from the hypothalamus as a whole in containing SS14 and SS28 in almost equimolar concentrations. The localized abundance of SS28 in the nerve terminals of the median eminence suggests a specific role for this peptide in the hypothalamic regulation of growth hormone secretion.

Amygdala↗
PubMed1986

Na-K-ATPase-inhibiting and glucose-6-phosphate dehydrogenase-stimulating activity of plasma and hypothalamus of the Okamoto spontaneously hypertensive rat.

The plasma of normal man and the rat, and an acetone extract of hypothalamus from the rat, have an ability to inhibit Na-K-ATPase which is related directly to salt intake. The ability of the plasma to inhibit Na-K-ATPase is raised in essential hypertension. The ability of plasma and of an acetone extract of hypothalamus from six spontaneously hypertensive (SHR) rats and six normotensive control (WKY) rats to inhibit Na-K-ATPase of fresh guinea-pig kidney was studied using cytochemical bioassay techniques. With a validated assay, which measures the capacity of biological samples to stimulate glucose-6-phosphate dehydrogenase (G6PD) as an index of their capacity to inhibit Na-K-ATPase, the mean G6PD-stimulating ability of the plasma from the SHR and the WKY rat was 772.3 +/- 48.1 units/ml and 12.5 +/- 2.6 units/ml respectively (P less than 0.01) and of the hypothalamic extracts it was 2.2 +/- 1.7 X 10(8) and 4.5 +/- 1.8 X 10(4) units/hypothalamus (P less than 0.01). With a semi-quantitative cytochemical assay, which measures Na-K-ATPase activity directly, plasma and an acetone extract of hypothalamus from the spontaneously hypertensive rat had much greater capacities to inhibit Na-K-ATPase than plasma and extract from the WKY rat. These raised levels of Na-K-ATPase inhibitory activity in the plasma of the SHR rat are similar to the highest values found in the plasma of patients with essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Thyrotrophin-releasing hormone-related polypeptides in rabbit prostate and semen are different from those in rabbit hypothalamus.

TRH-related peptides were extracted from the hypothalamus and prostate gland of the rabbit. The peptides were fractionated by gel exclusion chromatography and located by trypsin digestion and radioimmunoassay with antibodies to TRH amide and TRH-Gly Lys. In the hypothalamus TRH-related peptides containing approximately 16 and 30 residues were observed: in these peptides the extensions to the TRH sequence were exclusively in the C-terminal direction. In addition, the three-residue form of TRH was also present. In the prostate complex, the predominant TRH-related peptide contained approximately 50 residues and the extension to the TRH tripeptide was on the N-terminal side; a three-residue form of immunoreactive TRH was also demonstrated. The same pattern of TRH-related peptides was shown to be present in rabbit semen. The results reveal the existence of a novel TRH-related polypeptide in the prostate and semen which does not occur in the hypothalamus. This peptide appears to undergo secretion.

Animals↗
PubMed1993

Growth hormone (GH) suppression of catecholamine turnover in the chicken hypothalamus: implications for GH autoregulation.

GH administered centrally or peripherally inhibits basal or secretagogue-induced GH secretion in domestic fowl. Since the release of pituitary GH is neurally regulated by the hypothalamus, GH autoregulation may be mediated by changes in the content or metabolism of hypothalamic monoamines. When chicken GH (500 micrograms/kg body weight) was injected i.v. into laying hens, tissue catecholamine (adrenaline, noradrenaline and dopamine) concentrations in the preoptic area (POA) and medial basal hypothalamus (MBH) were depleted for 2-24 h, as were concentrations of dihydroxyphenylacetic acid, a dopamine metabolite. The serotonin (5-HT) content of the POA and MBH was unaffected by i.v. GH administration, although a reduction in MBH 5-hydroxyindoleacetic acid suggested a tissue-specific inhibition of 5-HT turnover. Qualitatively similar results were observed in laying hens 24 h after the intracerebroventricular injection of chicken GH (10 micrograms/bird). These results therefore demonstrate aminergic actions of GH within the chicken hypothalamus which may mediate GH autoregulation. However, as amine metabolism is not only suppressed when endogenous GH secretion is reduced, but also at times when normal GH secretion is restored, these aminergic effects may also reflect other actions of GH on central function.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

Rat placental lactogen-I binds to the choroid plexus and hypothalamus of the pregnant rat.

Recent findings suggest that placental lactogen has a role in the regulation of hypothalamic function during pregnancy. To explore the mechanisms by which placental hormones may exert effects in the maternal central nervous system, we have examined the binding of rat placental lactogen-I (rPL-I) to brain slices from pregnant rats at mid- and late gestation. The binding of rPL-I to maternal rat brain was compared with that of human GH (hGH). Radiolabelled rPL-I bound specifically to ependymal cells of the choroid plexus in the lateral ventricles and in the roof of the third ventricle. The binding of 125I-labelled rPL-I was inhibited by unlabelled rPL-I, hGH or rat prolactin but not by rat GH, indicating that rPL-I and rat prolactin interact with a common binding site in maternal rat brain. Radiolabelled hGH bound to the choroid plexus and to ependymal cells lining the third ventricle in the region of the arcuate nucleus. In addition, hGH bound specifically to the ventromedial nuclei and to the medial preoptic area of the hypothalamus. The binding of radiolabelled hGH to all brain regions was inhibited by unlabelled rPL-I as well as hGH, indicating that rPL-I competes for lactogenic binding sites in the hypothalamus as well as the choroid plexus of the pregnant rat. These findings suggest potential mechanisms by which placental hormones may exert direct effects on the maternal central nervous system during pregnancy. The precise functions and roles of the PL-I binding sites in maternal choroid plexus and hypothalamus remain to be explored.

Animals↗
PubMed1996

Changes in the binding characteristics of the mu, delta and kappa subtypes of the opioid receptor in the hypothalamus of the normal cyclic ewe and in the ovariectomised ewe following treatment with ovarian steroids.

The mu, delta and kappa opioid receptor subtypes were measured across the oestrous cycle of the ewe and in ovariectomised (OVX) ewes treated with oestrogen and/or progesterone. We have used a subtype-specific opioid receptor binding assay, in which [3H]diprenorphine non-preferentially labelled each receptor subtype in the presence of blocking concentrations of site-specific opioid analogues. The density and affinity of each receptor subtype was measured in the preoptic area (POA) of the hypothalamus and the mediobasal hypothalamus (MBH). Normally cycling ewes were killed during the luteal phase of the oestrous cycle and at various times after an injection of a synthetic prostaglandin (cloprostenol) to synchronise the onset of the follicular phase. OVX ewes were either untreated as controls (n = 4) or treated with oestrogen (n = 4), progesterone (n = 4) or oestrogen and progesterone combined (n = 4). The total number of opioid receptors did not alter across the oestrous cycle or with steroid hormone treatment. In the POA, the mean (+/- S.E.M.) number of delta receptors was significantly (P < 0.05) greater during the luteal phase than 24 h into the follicular phase (133 +/- 45 vs 35 +/- 8 fmol/mg protein). A significantly (P < 0.05) greater number of delta receptors was also found in the OVX progesterone-treated ewes compared with the control animals (172 +/- 9 vs 39 +/- 4 fmol/mg protein). In the MBH, the number of delta receptors was significantly (P < 0.01) greater in ewes killed 56 h after prostaglandin than luteal-phase ewes (184 +/- 40 vs 51 +/- 7 fmol/mg protein). The number of mu receptors in both the POA and the MBH was also significantly (P < 0.05) higher in the 56-h group than in the 12-h group. A similar trend was also observed in the steroid-treated animals, although differences did not reach statistical significance. The delta:mu ratio in the POA was significantly (P < 0.05) higher in the luteal-phase animals than any of the other groups killed after a cloprostenol injection that causes luteolysis. Similarly the ratio of delta receptor density to mu receptor density was greater (P < 0.05) in the OVX progesterone-treated ewes than in the OVX control ewes. No differences were found in the kappa receptor density across the cycle or with different steroid treatments. These data suggest that the relative proportions of the delta and mu subtypes of the opioid receptor in the hypothalamus change during the oestrous cycle. Regulation appears to be due to the feedback effects of ovarian steroids with progesterone altering the delta:mu ratio. In the MBH, there was a general increase in both delta and mu subtypes during the follicular phase of the oestrous cycle. This may explain, in part, how the responsiveness of the GnRH/LH axis to opioid peptides and antagonists changes across the cycle.

Animals↗
PubMed1995

Neurotransmitter interactions in the striatum and hypothalamus of mice after single and repeated ethanol treatment.

In single treatment study, ethanol was administered intraperitoneally to ICR mice (about 34 g) in the amounts of 1.0, 2.0, 3.0 or 4.0 g/kg body weight. The 3,4-dihydroxyphenylacetic acid (DOPAC) + homovanillic acid (HVA) concentration in the striatum was elevated with 3.0 and 4.0 g/kg of ethanol. In the hypothalamus, the DOPAC, HVA and 5-hydroxyindoleacetic acid concentrations were increased after injection of 3.0 and 4.0 g/kg of ethanol. Furthermore, the acetylcholine (ACh) and gamma-aminobutyric acid (GABA) concentrations were also increased following the injection of 1.0, 2.0, 3.0 and 4.0 g/kg. To study the effects of repeated administration, mice were injected intraperitoneally with 1.0 or 2.0 g/kg of ethanol once daily for 7 days. The DOPAC + HVA level in the striatum was elevated after injection of 1.0 and 2.0 g/kg of ethanol. The GABA and ACh concentrations in the hypothalamus were decreased after repeated injections of ethanol. These results suggest that ethanol significantly alters the utilization of dopamine, ACh and GABA in the hypothalamus. This may partially explain why ethanol has such profound effects on emotional behavior and mood.

Animals↗
PubMed1998

Castration differentially regulates nitric oxide synthase in the hypothalamus and pituitary.

Mammalian reproductive function is under control of the integrated hypothalamic-pituitary-gonadal (HPG) axis. Castration in male rats has been utilized as an effective tool to investigate hormonal interactions in the mammalian HPG axis. Recently, nitric oxide (NO) has been suggested to play a role in HPG hormonal regulation. In order to gain further insight into the function of the NO-NOS system in reproductive neuroendocrine control, particularly in the gonadal feedback regulation of the hypothalamic-pituitary unit, we examined steady state levels of nNOS mRNA, nNOS protein, and the important physiological index, NOS enzyme activity, of the intrinsic NOergic system in both hypothalamus and pituitary in castrated male rats and their sham-operated counterparts one week after surgery. In the pituitary, we found a significant four-fold increase in nNOS mRNA, p < 0.0003 compared to sham. Castration also resulted in a four-fold rise in pituitary nNOS protein, p < 0.02 compared to sham. Pituitary NOS enzyme activity was stimulated 2 fold, p < 0.003 after castration. In the hypothalamus, conversely, we observed no significant castration-modulated difference in either nNOS mRNA, nNOS protein or NOS enzyme activity. Thus, it appears that the hypothalamic NO-NOS system is either not required for hypothalamic adaptations to castration, although important in the release of LHRH under normal physiological conditions, or alternatively, the hypothalamus may become more sensitive to the effects of NO in the castrated state. In the pituitary, NO may attenuate the gonadotropin response to castration as a local balancing mediator.

Animals↗
PubMed1987

Progesterone and progestins modulate beta-endorphin concentrations in the hypothalamus and in the pituitary of castrated female rats.

Hypothalamic and pituitary beta-endorphin (B-EP) concentrations are modified by ovariectomy and estrogen treatments, supporting a direct interaction between this peptidergic system and gonadal steroids. Because the use of progestins is becoming even more diffuse in clinical practice, we evaluated the effect of progesterone and of the synthetic progestins medroxyprogesterone acetate (MPA), norethisterone acetate (NET) and desogestrel on the concentration of B-EP in the medial-basal hypothalamus and the anterior and neurointermediate pituitary lobes in ovariectomized rats (OVX), treated or untreated with estradiol benzoate (EB). B-EP concentrations were significantly increased by desogestrel in the anterior lobe and by progesterone, desogestrel and medroxyprogesterone acetate in the neurointermediate lobe. Progesterone and progestins significantly reduced B-EP increase induced by estradiol benzoate in the anterior lobe. Estradiol benzoate treatment did not modify the effect of progesterone and desogestrel on B-EP in the neuro-intermediate pituitary lobe. Norethisterone acetate and progesterone increased B-EP concentrations in the medial-basal hypothalamus, while the other steroids were inactive. In contrast, in the hypothalamus all progestins attenuated the increase of B-EP induced by estradiol benzoate (p less than 0.01). These data indicate that progesterone and progestins modulate the hypothalamic and pituitary B-EP concentrations in concert with estrogens. The capacity of progestins to modify the hypothalamic contents of B-EP may represent one of the mechanisms of action of these steroids in influencing brain function.

Animals↗
PubMed1981

Resolution of estrogen binding species in hypothalamus and pituitary.

In addition to the classic Type I estrogen receptor, a second estrogen binding species has been reported in rat uterine nuclear material. We have examined nuclear material from hypothalamus and pituitary for the presence of Type II estrogen receptor by the sucrose pad/exchange assay. Extensive (0.05-40.0 nM) saturation analyses were performed on crude chromatin isolated from hypothalami and pituitaries of hyperestrogenized ovariectomized rats. Analysis of data by an adaptation of the graphical method of Rosenthal suggests that there is only a single class of estrogen binding sites in these tissues with a Kd (0.2 nM) close to that reported for Type I receptors in other systems. However, a definitive resolution of the binding component(s) was not possible due to noise in the upper regions of the saturation plot. Therefore, we pooled 7 hypothalamic and 4 pituitary saturation experiments and analyzed the data with LIGAND, a nonlinear curve fitting program. Computer generated curves indicate that the data from both target tissues are approximated most closely by a model describing a single high affinity binding species (Type I) (Kd = 0.17 - 0.38 nM) and a linear or very low affinity nonspecific binding component. Thus, we conclude that there is no evidence for the presence of a second or lower affinity estrogen binding component in hypothalamus or pituitary. The absence of this binding species in these two estrogen target tissues is consistent with the concept that Type II sites may be involved in estrogen's control of tissue hypertrophy and hyperplasia--estrogen responses not found in hypothalamus or pituitary.

Animals↗
PubMed1975

[The role of the hypothalamus in the mechanism of positional nystagmus].

The typical positional nystagmus was induced in 30 intact rabbits with injection of 0.1-0.4 ml of 0.03-0.05% dicaine solution into the cerebral cisterna magna. The positional nystagmus resulted, supposedly, from the effect of the anesthetic upon the basal structures of the 3rd ventricle of the brain, upon the hypothalamus in particular. The trigger mechanism of the phenomenon is the displacement of the membraneous ampullae of semicircular canals at the tilting of the head. To prove this, 0.01-0.03 ml of 4% dicaine solution were injected directly into the anterior and posterior hypothalamus through a metallic cannula. When introduced into the anterior hypothalamus the dose of the anesthetic necessary for occurrence of the positional nystagmus is two or three times lesser than when it is injected into the posterior nypothalamus. In two delabyrinthed rabbits we failed to induce the nystagmus in this way.

Animals↗
PubMedDate not supplied

[Effect of testosterone on carboxypeptidase H activity in the murine hypothalamus and hypophysis].

Effects of single intraperitoneal administration of testosterone propionate (3 or 30 mg/kg body weight) on activity of carboxypeptidase H in pituitary body and hypothalamus of female white mouse were studied. It was found that testosterone propionate treatment (3 and 30 mg/kg body weight) increased the carboxypeptidase H activity in pituitary through 0.5 hour and it decreased one in 24 hours after treatment. The carboxypeptidase H activity in hypothalamus was lower as compared with control animals in 24 hours after testosterone propionate treatment in the dose 3 mg/kg body weight. However, the carboxypeptidase H activity in hypothalamus was lower in 0.5 and 24 hours and it was higher in 4 h after testosterone propionate treatment in the dose 30 mg/kg body weight as compared with the control. These data suggest that testosterone affects the carboxypeptidase H activity by changing the level of enzyme gene expression.

Animals↗
PubMed2000

Effects of melatonin on dopamine metabolism in the hypothalamus and the pituitary of the rainbow trout, Oncorhynchus mykiss.

The present paper discusses the effect of a single melatonin treatment (0.5 mg/kg, i.p.) on the dopaminergic metabolism in the hypothalamus and pituitary of the rainbow trout. The effects of exogenous melatonin on dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) contents were compared with the variations in the content of these catecholamines associated to the natural increase in the endogenous melatonin from daytime (3 hr before lights off) to nighttime (3 hr after lights off). Animals treated with melatonin showed a rapid (maximal values at 30 min post-injection) and relatively sustained rise in plasma melatonin levels, which reached supraphysiological ranges. The increase in circulating melatonin was accompanied by a reduction in the amount of DOPAC in both the hypothalamus (30, 60, and 120 min after i.p. melatonin) and the pituitary (120 min after i.p. melatonin) as well as in the pituitary DOPAC/DA ratio (60 and 120 min after i.p. melatonin). Similarly, the increase in circulating melatonin levels from the daytime to nighttime was associated with decreases in the contents of DOPAC in both the hypothalamus and pituitary and in the DOPAC/DA ratio in the pituitary. These data suggest that the inhibition of the hypothalamic-pituitary dopaminergic metabolism may be a specific mechanism of melatonin action in the trout brain that might operate following changes in the secretion of the hormone from the pineal gland.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

Luteinizing hormone-releasing hormone in thymus and hypothalamus of rat fetuses: suppressing effect of antagonist and of antibodies on concanavalin A-induced proliferation of thymocytes.

The effect of endogenous luteinizing hormone-releasing hormone (LHRH) on the proliferation induced by concanavalin A (Con A) in rat fetal thymocytes was studied. A selective antagonist (2 microg per fetus) or antibodies to LHRH (20 microl per fetus) were injected in utero into 20-day-old rat fetuses, and this resulted in a two- or fivefold decrease in the Con A-induced proliferation of thymocytes, respectively. In combined culture of the antagonist (10-5-10-6 M) with fetal thymocytes, the proliferative response was not decreased. The concentration of LHRH was determined by radioimmunoassay in tissues of immunocompetent organs and in blood serum of 18- and 21-day-old fetuses, and the hormone was found in the hypothalamus, thymus, and peripheral blood. The initially low level of LHRH in the thymus increased by 65 and 40%, respectively, on the first day after birth and became similar to the level in the hypothalamus. In the fetal blood serum, the LHRH level was significantly higher than in the thymus and hypothalamus of fetuses of the same age. The hormone concentration was greatest in the 18-day-old fetuses, and it decreased twofold by the 21st day. The findings indicate that LHRH is involved in regulation of T-cell immunity even during prenatal ontogenesis.

Animals↗