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PubMed1991

Colchicine-induced increases in immunoreactive neuropeptide levels in hypothalamus: use as an index of biosynthesis.

The colchicine-induced accumulation of vasopressin (AVP) and oxytocin (OXT) has recently been applied to estimate the synthesis and turnover rates for these neuropeptides in whole rat hypothalamus. In the present studies, this pharmacologic procedure has been examined as a potential method for estimating hypothalamic somatostatin (SRIF) synthesis rate, and evaluated further for its utility in estimating nonapeptide synthesis in individual hypothalamic nuclei. Adult male rats received a single injection of colchicine (8 micrograms) into the third ventricle under pentobarbital anesthesia. Twenty-four hr later, immunoreactive (IR) levels of AVP and OXT increased considerably, as previously noted. Hypothalamic IR-SRIF levels, however, were unaffected. The absolute increases in IR-AVP and IR-OXT were greatest in the supraoptic nucleus (SON), with smaller increments in the para/periventricular hypothalamus (PVH) and the median eminence (ME). IR-SRIF levels showed no changes in the PVH or the ME. As a test, the method was applied to the detection of changes in AVP synthesis in diabetic rats. The colchicine procedure reported increases in AVP synthesis in both the SON and PVH in diabetic animals, a result compatible with that obtained previously for whole hypothalamus using radiolabeled procedures. Together, the results indicate that the colchicine procedure is useful in detecting changes in the syntheses of some (AVP and OXT) but not all (SRIF) neuropeptides, and that when applicable, the method is sufficiently sensitive to detect changes in small hypothalamic regions. The method may prove useful in estimating changes in peptide synthesis analogous to that used for serotonin and dopamine; e.g., 5-hydroxytryptophan and dopa accumulation following inhibition of aromatic L-amino acid decarboxylase.

Animals↗

PubMed1983

Neurogenic hypertension after depletion of norepinephrine in anterior hypothalamus induced by 6-hydroxydopamine administration into the ventral pons: role of serotonin.

Destruction of the ventral noradrenergic pathway elicited by administration of 6-hydroxydopamine (6-OHDA, 5 micrograms into each side of the ventral pons) reduced the content of norepinephrine (NE) in the anterior hypothalamus (-80%) and induced an increase in arterial blood pressure (ABP) and in heart rate. These hypertensive rats, showed hypersensitivity to the hypotensive effect of NE (0.5-2 micrograms) and clonidine (0.75-1.5 micrograms) administered into the anterior hypothalamic preoptic (AH/PO) region. Methysergide (1-2 micrograms) and, to a lesser extent, ketanserin (1-2 micrograms) administered into the anterior hypothalamic preoptic region also reduced the arterial blood pressure in these rats treated with 6-OHDA. Bilateral administration of 5,7-dihydroxytryptamine (5,7-DHT, 8 micrograms) into the median forebrain bundle decreased the content of serotonin (5-HT) in the hypothalamus (-85%) without change in arterial blood pressure but largely prevented the development of hypertension after treatment with 6-OHDA in the ventral pons. These results suggest that neurogenic hypertension is produced after the removal of NE tonic depressor activity in the anterior hypothalamus and that serotonergic mechanisms play a major role in the development of the increased arterial blood pressure in this preparation.

5,7-Dihydroxytryptamine↗

PubMed1985

Comparative effects of infusions of 6-hydroxydopamine into nucleus accumbens and anterolateral hypothalamus induced by 6-hydroxydopamine on the response to dopamine agonists, body weight, locomotor activity and measures of exploration in the rat.

Groups of rats received infusions of 6-hydroxydopamine (6-OHDA) into the nucleus accumbens or anterolateral hypothalamus with 6-hydroxydopamine (6-OHDA), or sham operations. Body weight was monitored for 28 days after the infusion, after which rats were first tested in an exploration choice-box and then underwent a series of pharmacological challenges. At this time after the operation, rats which had received 6-OHDA in the nucleus accumbens showed neither loss of body weight, deficit in exploration, nor hypokinesia, but sustained an 80% reduction in dopamine levels in the nucleus accumbens. Locomotion was decreased in response to 1.5 mg/kg (i.p.) of d-amphetamine but increased following 0.1 mg/kg (s.c.) of apomorphine; stereotyped responses to larger doses were unaltered. By contrast, rats which had received 6-OHDA in the anterolateral hypothalamus lesions lost substantial amounts of body weight and were hypoactive. Although both locomotor and stereotypy responses to d-amphetamine were abolished, these responses were enhanced in response to apomorphine. Consistent with this, regional assay using high pressure liquid chromatography (HPLC) showed profound loss of dopamine in the caudate-putamen as well as in the nucleus accumbens and frontal cortex. It seems unlikely that the reductions in exploration previously reported after lesions of the mesolimbicocortical dopamine system at the level of anterolateral hypothalamus induced by 6-OHDA are either behaviourally specific or result solely from depletion of dopamine with the nucleus accumbens and frontal cortex.

Animals↗

PubMed1993

Antagonism of central pressor response to angiotensin II by alpha-human atrial natriuretic polypeptide at the preoptic area and posterior hypothalamus in rats.

Effects of alpha-human atrial natriuretic polypeptides (alpha-hANP) on pressor responses to angiotensin II (AII) were assessed at the preoptic area, posterior hypothalamus and central amygdaloid nucleus (ACE) in spontaneously hypertensive (SHR) and control normotensive Wistar-Kyoto (WKY) rats. Angiotensin II, administered intracerebroventricularly, at a dose of 100 ng produced a marked pressor response in hypertensive, as well as in normotensive rats and the response was potentiated in hypertensive rats. The response was antagonized in a dose-dependent manner by administration of alpha-hANP into the preoptic area and posterior hypothalamus but not to the amygdaloid nucleus. The antagonism was more marked in hypertensive than in normotensive rats. Angiotensin II, when injected directly to the preoptic area at a small dose of 10 ng similarly evoked a marked pressor response, which was augmented in hypertensive rats. This response was also antagonized by coadministration of alpha-hANP to the preoptic area in hypertensive but not in normotensive rats. The results suggest that the antagonistic relationship between ANP and AII exists at the preoptic area and posterior hypothalamus, probably implying that the activity of the ANP and AII systems in brain play a role in centrally controlling the cardiovascular system and is altered at these areas in genetically hypertensive rats.

Amygdala↗

PubMed1984

Rearing rats with mice prevents induction of mouse killing by lesions of the septum but not lesions of the medial hypothalamus or medial accumbens.

Rats which had been reared with mice and those which had not were subjected to lesions of the septum, medial accumbens, medial hypothalamus, or sham lesions. Forty-eight hours later all animals were presented with a mouse and the frequency of mouse killing recorded. In rats with lesions of the septum, the lesions induced killing only in those animals which had not been reared with mice. Rats with lesions of the medial accumbens or medial hypothalamus killed significantly more often than control animals even when they had been reared with mice. These results suggest that the septum, medial accumbens and medial hypothalamus subserve different functions in the inhibitory modulation of mouse killing behavior.

Animals↗

PubMed1985

Meal-stimulated increased concentrations of beta-endorphin in the hypothalamus of Zucker obese and lean rats.

Increased opiate peptide concentrations in brain and plasma have been associated with increased feeding. The role of beta-endorphin in the control of food intake and obesity was examined by measuring concentrations in hypothalamus, pituitary and plasma of hungry (6-hr fasted) and satiated (5 min after a meal) Zucker obese and lean rats. beta-Endorphin concentrations (1) in satiated vs. hungry rats were increased in the VMH (90 vs. 79 pg/mg tissue, p less than 0.05) and decreased in the supraoptic nucleus (65 vs. 78 pg/mg tissue, p less than 0.05), (2) in obese vs. lean rats were decreased in the VMH (79 vs. 90 pg/mg tissue, p less than 0.05) and (3) in female vs. male rats were increased in the anterior hypothalamus (123 vs. 59 pg/mg tissue, p less than 0.01) and VMH (90 vs. 79 pg/mg tissue, p less than 0.05). Analysis of a phenotype by feeding condition interaction revealed that obese but not lean rats had higher beta-endorphin concentrations in the satiated vs. hunger condition. However, plasma beta-endorphin concentrations did not differ with feeding condition, phenotype or sex. Intermediate and posterior but not anterior pituitary beta-endorphin concentrations were lower in obese than lean rats. Thus, there is some evidence for a relationship between beta-endorphin concentration and feeding in the hypothalamus, but beta-endorphin concentrations in plasma do not appear to be influenced by feeding condition or obesity.

Animals↗

PubMed1993

Offense produced by chemical stimulation of the anterior hypothalamus of the rat.

Offense behavior, including bite-and-kick attack, was obtained by microinjections of picrotoxin into the anterior hypothalamus of the rat. This is the first time that it has been possible to obtain offense by chemical stimulation of the brain, and the localization is more precise than that obtained with electrical stimulation. Mounting behavior and mounting by the opponent were also obtained from the anterior hypothalamus, the former corresponding to results obtained by previous studies using electrical stimulation. Other behaviors obtained from the hypothalamus included locomotion and circling, social and self-grooming, upright posture and boxing, digging, feeding, and leaping.

Aggression↗

PubMed1986

Structural changes induced in capillary endothelial cells by growth factors: altered distribution of cytoskeletal elements and organelles in cells spreading in the presence of tumor conditioned medium and hypothalamus derived growth factor.

Using high-voltage and conventional electron microscopy of cell whole mounts, we have investigated the effects of tumor-conditioned medium and hypothalmus-derived growth factor on the structure of capillary endothelial cells during their attachment and spreading in tissue culture. Cells were cultured in A, Dulbecco's Modified Eagle's Medium (DMEM) and 10% calf serum; B, equal parts of A and 48 hr mouse sarcoma conditioned medium; and C, A containing 10 units of hypothalamus-derived growth factor. Cells cultured in all three media were fully spread, and to the same extent, by 4 hr after plating. While spreading, cells cultured in DMEM alone developed prominent stress fibers and contained numerous bundles of microtubules which formed radical tracts along which mitochondria and other organelles rapidly moved to the cell periphery. Stress fibers were thinner and microtubule tracts fewer in number in cells cultured in tumor-conditioned medium. In 4 hr, organelles moved only part of the distance to the cell margin. Stress fibers were rudimentary and microtubules randomly orientated in cells exposed to hypothalamus-derived growth factor. Most organelles remained near the cell nucleus. The dramatic decrease in stress fibers and microtubule tracts in cells grown in tumor-conditioned medium and hypothalamus-derived growth factor and the subsequent decreased capacity of the cells to move organelles toward their periphery could have some functional significance relative to the growth-promoting activity of these substances.

Adrenal Glands↗

PubMed1983

Effects of psychotropic drugs microinjected into the hypothalamus on muricide, catalepsy and cortical EEG in OB rats.

In order to elucidate the mechanism of anti-muricide action of psychotropic drugs in the brain, the present study examined influences of these drugs microinjected into the hypothalamus on muricide. Inhibition of muricide by chlorpromazine (CPZ) was found both in the lateral preoptic area (1-POA) and the posterior part of the lateral hypothalamus (p-LH), and that by chlordiazepoxide was seen only the mammillary body. These effects were accompanied by a drowsiness of cortical EEG. Anti-muricide action of tricyclic antidepressants was found in p-LH. The effect was not accompanied by EEG drowsiness. Effects of atropine injected into the hypothalamus on muricide and cortical EEG were similar to those of the antidepressants. Norepinephrine and serotonin did not show selective muricide-suppression. Although either CPZ in 1-POA and p-LH or the antidepressants in p-LH showed cataleptogenic effect, these effects did not appear related to anti-muricide action. The relationship between the anti-muricide action of psychotropic drugs and the physiological functions of the brain was discussed in comparison with these systemic administrations.

Aggression↗

PubMed1990

Ouabain injected into the hypothalamus elicits pressor responses in anaesthetized rats: a mapping study.

Cardiac glycosides are known to have a narrow therapeutic index, due in part to their effects on the brain. Injections of cardiac glycosides into the ventricles of the brain elicit activation of the autonomic nervous system, and may even elicit cardiac arrhythmias. However, the specific brain regions responsible for such action are unknown. The hypothalamus receives chemo- and baro-receptive innervation from the cardiovascular system. In turn, there are both direct and indirect effector pathways from the hypothalamus accessing the sympathetic preganglionic and parasympathetic ganglia regions. This suggests that the hypothalamus may be a prime candidate for the central toxic effects of cardiac glycosides. The purpose of this experiment was to map the rostral diencephalon to determine sites at which injections of a low dose of the cardiac glycoside, ouabain, resulted in altered cardiovascular responses in the anaesthetized rat. Microinjections of 20 ng of ouabain in 200 nl were made into sites throughout the rostral diencephalon of urethane (1.2 g/kg) anaesthetized rats while monitoring heart rate and blood pressure. Injections into the nucleus medianus, paraventricular, anterior and posterior hypothalamic nuclei produced increases in pressure of from 5 to 25 mmHg. These data suggest that part of the toxicity resulting from the cardiac glycoside administration may be due to the direct action of the glycosides on these hypothalamic structures. The paraventricular region has the greatest sensitivity and may be a primary target due to its direct connections with the preganglionic sympathetic regions in the spinal cord.

Anesthesia↗

PubMed1986

PAP complex: a pitfall in immunocytochemistry of the pig hypothalamus.

Use of rabbit peroxidase-antiperoxidase (PAP) complex in immunostaining of the pig hypothalamus resulted in false positive staining of elements of the supraoptic and paraventricular nuclei due to binding of rabbit PAP complex and rabbit immunoglobulins to these structures. This phenomenon seriously hampers immunohistochemical investigation of the pig hypothalamus. Specific binding of swine immune serum against luteinizing hormone-releasing hormone has been detected with the protein A-biotin-streptavidin method employed on paraffin and vibratome sections of fetal and postnatal pig hypothalamus.

Animals↗

PubMed1987

A simple, sensitive method for the determination of extracellular catecholamines in the rat hypothalamus using in vivo dialysis.

The design, construction and characterisation of a dialysis probe suitable for perfusing any deep brain structures is described. Using high-performance liquid chromatography with electrochemical detection (HPLC-ECD) the effects of flow rate, concentration, dialysate composition and temperature on the recovery within the dialysate of authentic catecholamines are detailed. The dialysis probe was used to collect endogenous catecholamines from the anterior hypothalamus of urethane-anaesthetised rats. Following organic phase extraction of the in vivo samples, a small basal release of noradrenaline (NA) of 37 +/- 4 pg/30 min sample was found. Potassium stimulation markedly elevated the release of NA and dopamine from the anterior hypothalamus in a calcium ion and dose dependent manner. It appears therefore that the dialysis probe described here, in conjunction with HPLC-ECD, can be used to follow changes in neuronally released catecholamines within the anterior hypothalamus, providing a valuable tool to study the role of these neurotransmitters in physiological and pharmacological function.

Animals↗

PubMed1992

Pulsatile release of histamine in the hypothalamus of conscious rats.

The pattern of histamine release was investigated in the hypothalamus of the conscious, freely moving rat over 20 h. Under anaesthesia, a guide cannula was stereotaxically inserted into the posterior hypothalamus. In the conscious animal, the stylet of the guide cannula was replaced by a push-pull cannula, and the hypothalamus was superfused with artificial cerebrospinal fluid. Histamine was determined radioenzymatically in the superfusate which was continuously collected in time periods of 20 min. The release rate of histamine fluctuated according to an ultradian rhythm (frequency: 1 cycle per 83 min) and a circadian rhythm with the highest release rate of histamine between 11:00 p.m. and 1:00 a.m. The release rate of histamine during darkness was higher than that during the light period. The results demonstrate that, in the brain, neuronal histamine is released according to rhythms with various frequencies.

Animals↗

PubMed1988

Ontogenetic development of the 5 alpha-reductase in the rat brain: cerebral cortex, hypothalamus, purified myelin and isolated oligodendrocytes.

In the central nervous system of the rat, the 5 alpha-reductase, the enzyme which converts testosterone into dihydrotestosterone, appears to be concentrated in the white matter and in particular to be associated with myelin. In order to verify whether a temporal correlation might exist between the formation of myelin membranes and the variations of the 5 alpha-reductase activity observed in the brain, the enzymatic activity was studied in the cerebral cortex and in the hypothalamus of male rat in the age range of 3-60 days, in myelin purified from animals of 15-60 days of life and in oligodendrocytes (i.e. in the cells responsible for the formation of the myelin) isolated from the brain of adult and very young rats (7th day of life, when the myelination process is not yet initiated). The results show that the formation of 5 alpha-androstane-17 beta-ol-3-one (DHT) in the cerebral cortex and in the hypothalamus has a peak activity in the first two weeks of life, before the beginning of the myelination process; purified myelin has an enzymatic activity always much higher than that present in the cerebral cortex and in the hypothalamus and shows a peak in the formation of DHT in the first period of myelinogenesis, on the third week of life. Finally the oligodendrocytes of young rats possess a much higher ability to convert testosterone into the 5 alpha-reduced metabolites than the oligodendrocytes of adult animals. A possible involvement of this enzyme in the myelin function may be hypothesized.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗

PubMed1989

On the distribution and morpho-functional characteristics of 5-HT-immunoreactive cells in the hypothalamus of fetuses and neonatal rats.

This study attempted to visualize serotonin (5-HT)-immunoreactive (IR) neurons in the hypothalamus of intact fetuses (E18) and neonatal rats (P9) as well as after their pretreatment with some drugs interfering with the 5-HT metabolism and uptake in the serotoninergic neurons (L-tryptophan, pargyline, 5-hydroxytryptophan, fluoxetine). The 5-HT-IR cells were not observed in the hypothalamus of normal, untreated fetuses and neonatal rats. However, two large accumulations of 5-HT-IR neurons appeared in the anterolateral hypothalamus and in the dorsomedial nucleus after the subsequent injections of the monoamine oxidase inhibitor, pargyline, and the amino acid precursor of the 5-HT synthesis, L-tryptophan. A significantly less intensive reaction was observed after injections either of the second precursor of the 5-HT synthesis, 5-hydroxytryptophan instead of L-tryptophan, or pargyline only. Immunostaining, provoked by the pargyline and L-tryptophan pretreatment, was completely blocked by the injection of the specific 5-HT uptake inhibitor, fluoxetine. It means that the 5-HT immunostaining of the hypothalamic neurons may be accounted for by their capacity to take up specifically 5-HT from the environment rather than by its intraneuronal synthesis from L-tryptophan. Nevertheless, the 5-HT synthesis from 5-hydroxytryptophan in these cells cannot be excluded. The uptake of extracellular 5-HT into catecholaminergic neurons can be excluded as nomifensine, the specific inhibitor of the uptake to these neurons, did not modify the immunostaining.

Animals↗

PubMed1990

Estrogen-independent and estrogen-induced progesterone receptors, and their regulation by progestins in the hypothalamus and pituitary of the chick embryo: an immunohistochemical study.

The effects of an anti-estrogen and of progestins on the progesterone receptor (PR) in the hypothalamus and pituitary of 10-day-old chick embryos were studied by immunohistochemistry with an antibody to the receptor. In a first experiment, to determine if endogenous estrogens are responsible for the early appearance of PR in the chick embryo, a continuous treatment with the anti-estrogen. Tamoxifen, was applied from day 0 of incubation. In the hypothalamus and pars distalis of the pituitary a Tamoxifen treatment (10 micrograms every other day from day 0) did not modify the distribution of PR-positive cells or the intensity of PR immunoreactivity (PR-IR), compared to oil-injected embryos. In contrast, the same treatment totally blocked the increase of PR-IR in embryos administered estradiol (10 micrograms on day 7). Thus, the estradiol-induced PR-IR is inhibited by Tamoxifen, whereas the natural appearance of PR is not. We conclude that, in the chick embryo, the basal expression of PR is estradiol independent. In a second experiment, the regulation of PR by its own ligands (progesterone and the synthetic progestin, R5020) was studied. Progesterone (150 micrograms), administered to embryos 16 or 48 h before sacrifice on day 10, induced a slight increase in PR-IR in hypothalamus and anterior pituitary, whereas R5020 had no effect. In embryos treated with estradiol on day 7, R5020 decreased the PR-IR to a level comparable to that of control embryos. Thus R5020, a non metabolizable progestin, down-regulates the estradiol-induced PR-IR, but has no effect on the estradiol-independent, naturally expressed PR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Developmental expression of the growth hormone receptor gene in the rat hypothalamus.

The ontogeny of growth hormone receptor (GHR) gene expression was studied in the rat hypothalamus. Total RNA from the hypothalamus of rats at different developmental stages (embryonic day 15-56 days of age) was characterized using a 32P-labeled RNA probe derived from the extracellular domain of the rat GHR cDNA. Two RNA species, 4.5 kilobases (kb) encoding for GHR and 1.2 kb encoding for GH-binding protein, were detected in hypothalamic tissue from embryonic day 15 to 56 days of age. Their levels were low at embryonic day 15 and increased toward 3 days of age. The level of 4.5-kb transcript preferentially increased from 7 days after birth, and it was maintained until 35 days of age. Thereafter, the level of 4.5-kb transcript declined. The ratio between the 4.5- and 1.2-kb transcripts was less than 2.0 from embryonic day 15 to 3 days after birth, while it was larger than 4 after 7 days of age. There was no sex difference in the levels or the ratios of the transcripts of the GHR gene from 7 to 56 days of age. The findings indicate that the 4.5-kb transcript preferentially processed postnatally in the rat hypothalamus.

Animals↗

PubMed1993

Ontogeny of prodynorphin gene expression in the rat hypothalamus.

Opioid peptides, deriving from prodynorphin, proenkephalin and proopiomelanocortin genes, have been shown to modulate brain development. Prodynorphin gene expression was studied here by in situ hybridization in the developing rat hypothalamus using oligodeoxynucleotide probes. Prodynorphin mRNA-synthetizing cells were observed in the ventromedial hypothalamic nucleus, the supraoptic and the paraventricular nuclei from embryonic days 16, 18 and 21, respectively. We detected no transient expression of prodynorphin gene in the rat hypothalamus. Prodynorphin mRNA-containing cells were also observed prenatally in the striatum, the cortex, the hippocampus and the amygdala. When compared with data from the literature, our results suggest that translation may immediately follow transcription of prodynorphin gene in the supraoptic nucleus. The presence of prodynorphin mRNA in the developing rat hypothalamus also raises the possibility of an involvement of prodynorphin-derived peptides in developmental processes and/or in the maturation of adult neural regulations.

Animals↗