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N Parvizi

Publications and source records attributed to N Parvizi.

At least 55 records · Page 3Linked to original sources
PubMed1985

Autoradiographic determination of catechol estrogen binding sites in brain, pituitary and uterus.

The anatomical pattern of nuclear binding of 2-OH[6,9-3H]estradiol ([3H]2-OHE2) in brain, pituitary and uterus have been studied autoradiographically. Autoradiograms of forebrain, pituitary and uterus show nuclear concentrations of radioactivity in certain cells. This nuclear concentration is abolished when unlabelled 2-OHE2 or E2 was injected prior to the injection of [3H]2-OHE2. In the brain nuclear labelling is observed in the septal-preoptic region, in the anterior hypothalamic area, and in the central hypothalamic area. Some estrogen-sensitive nuclear groups, such as lateral septum and hippocampus, do not show accumulation of radioactivity. In the uterus, luminal and glandular epithelium, stromal cells and muscle cells are labelled. A comparison of the quantitative nuclear uptake of radioactivity and of the different time intervals after the injection of different doses shows similar uptake of nuclear radioactivity. This is comparable to data obtained after [6,7-3H]estradiol ([3H]E2) injection. The results provide clear evidence for nuclear binding of catechol estrogens of the same magnitude as [3H]E2 after in vivo treatment.

Animals↗
PubMed1985

The vasopressin response to microinjections of norepinephrine into the brain of the conscious pig.

The possibility that the amygdala influences the release of vasopressin has been raised by the observation that electrical stimulation of this area results in vasopressin release in the conscious animal. Therefore the effect on vasopressin concentrations has been studied by microinjections of norepinephrine into the amygdala of the conscious miniature pig. The studies were performed on castrated male and female pigs with chronically implanted cannulae in the brain and in the external jugular vein. Lysine vasopressin concentrations were determined using a specific sensitive radioimmunoassay. Microinjections of 1 microliter 0.12 M sodium chloride were without effect. Injections of norepinephrine in the dose range 10(-4)-10(-10) M had no effect in the male animal but a significant vasopressin response could be obtained in the females.

Amygdala↗
PubMed1983

Catecholestrogens in the brain: neuroendocrine integration.

In a series of experiments it has been shown that 4-hydroxyestradiol (4-OHE2) as well as 2-hydroxyestradiol (2-OHE2) are involved in regulatory mechanisms of LH secretion in the miniature pig. Two-hydroxyestrone (2-OHE1) and 1-hydroxyestradiol-benzoate (1-OHE2B), however, have no significant effects on LH secretion. Moreover the studies indicate a regional specificity in the action of 4-OHE2, 2-OHE2 and estradiol (E2). 4-OHE2 and 2-OHE2 decrease plasma LH when given into the ventromedial nucleus of the hypothalamus and increase plasma LH levels when microinjected into the dorsomedial nucleus of the hypothalamus. Whereas E2 affects LH secretion when it is given into the area dorsalis of the hypothalamus and fornix. In addition the experiments performed on female and male rats to measure the effects of 2-OHE2 and 2-OHE1 on turnover rates of dopamine, norepinephrine and epinephrine in the anterior mediobasal hypothalamus and medial preoptic area show that the effects of catecholestrogens may partly be mediated by catecholamines.

Animals↗
PubMed1983

Catecholestrogens affect catecholamine turnover rates in the anterior part of the mediobasal hypothalamus and medial preoptic area in the male and female castrated rat.

To study the interactions of catecholestrogens with the catecholamine system we estimated the catecholamine concentrations and turnover rates in the anterior part of the mediobasal hypothalamus (AMBH) and medial preoptic area (MPO) following 2-hydroxyestradiol-17 beta (2-OHE2) or 2-hydroxyestrone (2-HOE1) treatment in castrated male and female rats. Serum concentrations of LH and prolactin were also measured. The turnover rates of catecholamines were calculated by monitoring the catecholamine loss 1 h after blocking the catecholamine synthesis with alpha-methyl-p-tyrosine. Dopamine, epinephrine and norepinephrine concentrations were measured by a radioenzymatic assay. In males, 2-OHE2 (50 micrograms/kg) and 2-OHE1 (50 micrograms/kg) resulted in decreased serum LH values (p less than 0.05) 4 and 5 h after treatment. None of these 2-hydroxylated estrogens were able to alter serum prolactin levels significantly. There was a decline in epinephrine and norepinephrine concentrations in the AMBH. The greatest change in catecholamine turnover rates in response to catecholestrogen treatment also occurred in the AMBH. 2-OHE2 and 2-OHE1 reduced turnover rates of dopamine, norepinephrine and epinephrine in the AMBH. Only the dopamine turnover rate was affected in the MPO, where it increased following 2-OHE2 treatment. In females, only 2-OHE2 (50 micrograms/kg) was effective in decreasing serum LH (p less than 0.05) and increasing prolactin (p less than 0.01) levels. Dopamine and epinephrine concentrations as well as their turnover rates declined in the AMBH after treatment with catecholestrogens. The concentration and turnover rate of epinephrine also decreased in the MPO. There was no significant change in norepinephrine concentration or turnover rate. It is suggested that 2-hydroxyestrogens are possibly involved in mechanisms which are inhibitory to LH secretion and stimulatory to prolactin release. These actions appear to be partly mediated by catecholamines.

Animals↗
PubMed1983

Anovulation in female rats induced by neonatal administration of the catechol estrogens, 2-hydroxy-estradiol and 4-hydroxy-estradiol.

The effects of estradiol (E2) and its 2- and 4-hydroxylated metabolites on gonadotrophin regulation in the female rat brain were examined. Neonatal female rats were injected from day 1 through 5 with E2, 2-OHE2 and 4-OHE2, at doses of 0.1, 1 and 10 micrograms/day. At 2, 6 and 24 h after the last estrogen injection, some animals from each treatment group were killed and the concentration of estrogen receptors (ERn) in their brain cell nuclei determined. The remaining animals were allowed to mature. Their vaginal smear patterns were examined from 7 to 9 and from 15 to 17 weeks of age. They were then ovariectomized and tested for their capacity to exhibit a luteinizing hormone (LH) surge in response to estrogen and progesterone injections. In a parallel series of experiments, the affinities of the three test estrogens for alpha-fetoprotein (AFP) were determined from in vitro competition studies with fetal rat serum. All three estrogens increased brain cell nuclear ERn concentrations, measured at 2 h after the final injection. E2 was more potent in this respect than either 4-OHE2 or 2-OHE2. E2 and 4-OHE2 competed for binding to AFP to an approximately equal extent. 2-OHE2, however, was a much weaker competitor for AFP than either of the other two compounds. The neonatal E2 and 4-OHE2 treatments reduced the number of animals showing regular cyclic vaginal smears, at all three doses tested. In contrast, 2-OHE2 significantly affected vaginal cyclicity only at a dose of 10 micrograms/day.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Ontogeny of hypothalamus-pituitary function in the fetal pig: gonadotropin release in response to electrical and electrochemical stimulation of the hypothalamus.

The ontogeny of hypothalamic control of anterior pituitary gonadotropin secretion was studied in anesthetized fetal pigs at different gestational ages (60, 80, and 105 days gestation; term, 114 days). Three or four fetuses from one mother simultaneously received either no treatment (control), sham operation, electrical stimulation (EL), or electrochemical stimulation (EC). Electrodes were implanted unilaterally into the hypothalamus. Fetuses remained in utero during surgery. A distinct difference in the development of basal LH and FSH secretion was observed. Basal plasma LH concentrations almost doubled (P less than or equal to 0.001) between days 60 and 80, with no further significant increase between 80 and 105. Plasma FSH concentrations did not change significantly between days 60 and 80, but increased more than 5-fold (P less than or equal to 0.001) between days 80 and 105. EL or EC did not affect LH secretion at 60 days. At 80 days, EL and EC significantly (P less than or equal to 0.05) elevated plasma LH concentrations 30 and 50 min after the onset of stimulation. At 105 days, EL and EC caused a rise in plasma LH levels within 10 min; the maximum level, reached 30 min after the onset of stimulation, was double that in 80-day-old fetuses. Plasma FSH values were not significantly affected by EL or EC in any age group. The results indicate that the fetal pig hypothalamus is able to influence pituitary LH secretion by day 80 (70% of gestation). Further, maturation of hypothalamic control of LH secretion becomes demonstrable between days 80 and 105. The development of hypothalamic control of FSH secretion is delayed relative to LH.

Animals↗
PubMed1982

Response of luteinizing hormone and follicle-stimulating hormone to luteinizing hormone releasing hormone in the fetal pig.

The responses of anesthetised fetal pigs (n=95) and chronically catheterized fetal pigs (n=10) to luteinizing hormone releasing hormone (LHRH) administration (2 micrograms/kg estimated fetal body weight) was investigated. Fetuses were studied at 55, 70, 85, 100, 106 (chronic) and 113 days. Plasma concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured by radioimmunoassay. Blood samples were taken from the umbilical artery (anesthetised fetuses) or carotid artery (catheterized fetuses) every 10 min for 1 h except in the youngest age group. No significant sex difference in the LH response to LHRH treatment was observed. The LH response increased with gestational age; average pretreatment plasma concentrations were below 1.1 ng/ml. No response was observed at 55 days, and the highest response was seen at 113 days when plasma LH concentrations rose to 4.3 +/- 0.7 (mean +/- SEM) ng/ml 40 min after treatment. Pretreatment plasma FSH concentrations at 55 days were 1.6 +/- 0.1 ng/ml and gradually rose in males to 3.2 +/- 0.4 ng/ml at 113 days, which was significantly lower than in females where concentrations averaged 8.1 +/- 2.0 ng/ml. LHRH did not significantly affect FSH concentrations in males, while in females a gradually increasing response was observed; at 113 days plasma FSH was 12.5 +/- 2.9 ng/ml 40 min after treatment. The increase in response to LHRH with age of plasma LH concentrations in both sexes, and of plasma FSH concentrations in females indicates the maturation of the hypothalamo-pituitary system.

Animals↗
PubMed1982

Further evidence on dual effects of norepinephrine on LH secretion.

To investigate the effects of norepinephrine (NE) on LH secretion, when given into different hypothalamic and extrahypothalamic brain regions, we microinjected 1 microliter of NE in dosages of 10(-4) M concentrations, 10(-6), 10(-8) and 10(-10) M into nine different brain areas in ovariectomized miniature pigs. Microinjections into the dorsal hypothalamus (ADH) and dorsomedial nucleus (DM) had dose-dependent effects. The higher dose of NE (10(-6) M) inhibited and the lower dose of NE (10(-10) M) stimulated LH secretion, when NE was microinjected into the ADH (n = 4 - number of animals). Microinjections into the DM (n = 6) had the opposite effect. Here the lower dose had inhibitory and the higher dose stimulatory effects on plasma LH levels. Microinjections into the ventromedial nucleus of the hypothalamus (n = 4) had no significant effect. Microinjections into the stria terminalis (n = 3) and zona incerta (n = 4) were also ineffective. The effect of NE microinjections into the subthalamic nucleus (n = 4) resembled responses to microinjections into the ADH. NE effects in the amygdala were not dose dependent. Microinjections into the basolateral amygdala (n = 5) decreased and microinjections into the corticomedial part of the amygdala (n = 5) increased plasma LH levels in all four doses of NE. The effects of NE microinjected into the hippocampus (n = 3) were not clear cut. These results indicate a dualism of NE on LH secretion. Thus, the predominant notion that NE is largely or even exclusively stimulatory to LH release should be revised. According to the previous findings and the results of the present study it has been concluded that the effects of NE on LH secretion are not only dependent on the hormonal status of the animal, but also to the dose and site of action of NE.

Animals↗
PubMed1980

beta-Endorphin alters luteinizing hormone secretion via the amygdala but not the hypothalamus.

Morphine and enkephalins are able to alter pituitary hormone secretion. It has been postulated that they do not act directly at the pituitary, but rather that the hypothalamus is the site at which inhibition or stimulation of pituitary hormone secretion is initiated. On the other hand, endogenous opiates have been located in distinctly different neuronal regions, including areas outside the hypothalamus. The effects of beta-endorphin on plasma luteinizing hormone (LH) levels have not been explored, and the present experiments attempt to elucidate the contribution and the possible site of action of beta-endorphin in the control of LH secretion. The results show that beta-endorphin inhibits pituitary LH secretion if applied into the amygdala but not when given into the hypothalamus.

Amygdala↗
PubMed1980

Gonadal steroids in the amygdala--differential effects on LH.

The direct participation of sexual steroids in the amygdala (AMY)-dependent modulation of LH secretion was investigated by means of a combination of microinjectons into the AMY and electrical stimulation of the AMY. Adult castrated male miniature pigs provided with bilateral 'electro-tubes' into the AMY were used. Electrical stimulation of the AMY without any prior steroid microinjection or with solvent microinjection decreased plasma LH levels. In contrast, electrical stimulation, 3.5 h after microinjection of 60 ng testosterone, resulted in an increase in LH levels. However, prior microinjection of estradiol-17 beta (6 ng) or 5 alpha-dihydrotestosterone (60 ng) abolished the effects of electrical stimulation. Four out of 7 of the animals responded to microinjection of 2-hydroxyestradiol-17 beta (60 ng) with a fall in plasma LH levels. Electrical stimulation increased the LH levels up to those before microinjection in these animals. In the other half of the animals, with no response to catecholestradiol microinjection, the response to electrical stimulation was depression. The results suggest a direct and differentiated effect of steroids on the AMY; the action of testosterone is independent of its aromatization or reduction and steroids could act on the AMY to inhibit or stimulate the inhibitory role of the amygdala in the control of pituitary LH secretion.

Amygdala↗
PubMed1980

Partial recovery of the stimulatory oestrogen feedback action on LH release during late lactation in the pig.

The functioning of the stimulatory oestrogen feedback mechanism during lactational anoestrus of the sow was evaluated by determining the LH response to a single i.m. injection of oestradiol benzoate. Oestradiol-17 beta and progesterone levels were also measured following treatment and following weaning. On Day 5 of lactation there was no LH response to oestradiol benzoate but on Day 35 of lactation a small but significant (P less than or equal to 0.05) increase in plasma LH occurred, and this was followed by a rise in plasma progesterone in 4 out of 9 animals 8 or 13 days later. It is concluded that blockade of the stimulatory oestrogen feedback mechanism is one cause of lactational anoestrus in the sow.

Animals↗
PubMed1979

Plasma oxytocin and steroid concentrations during late pregnancy, parturition and lactation in the miniature pig.

Plasma oxytocin concentrations were measured during late pregnancy, parturition and lactation in the miniature pig. Measurements were made of plasma oestradiol, oestrone and progesterone to determine whether there was any relationship between the concentrations of oxytocin and these steroids in the circulation. Plasma oxytocin concentrations were low or undetectable in late pregnancy. Rises of up to 68.8 mum./ml were seen at the time of delivery of the foetuses and at the expulsion of the placenta. The only steroid that seemed to relat to oxytocin release was progesterone. Oxytocin release was consistently seen when progesterone concentrations had fallen to below 10 ng/ml but no increase in concentration was observed while oestrone and oestradiol increased to their maximum concentrations of 3.86--11.6 and 0.43--0.70 ng/ml respectively. During lactation, when both oestrogen and progesterone concentrations were low, suckling caused the levels of oxytocin to increase to 7.4 muu./ml. These increases were greater during the first 2 weeks of lactation than later.

Animals↗
PubMed1978

Steroid feedback on luteinizing hormone secretion during sexual maturation in the pig.

The effects of gonadal secretions on the release of LH and the stimulation of LH secretion by oestradiol have been investigated in newborn male and female miniature pigs; the differences in the feedback action of testosterone in newborn and pubertal male pigs were also studied. Hemi-orchidectomy or orchidectomy of 1-week-old pigs had no effect on the level of LH in the plasma; total orchidectomy significantly reduced the levels of testosterone (P less than 0.01) and progesterone (P less than 0.05). In female pigs ovariectomized at 1 week of age, the concentration of LH in the plasma decreased, with a strong negative correlation between the level of LH and age (r = -0.41; P less than 0.05). The plasma concentration of progesterone was generally low and unaffected by ovariectomy. Orchidectomy and treatment of male pigs, at 1 week of age, with testosterone (6 mg/kg body weight) had no effect on the plasma concentration of testosterone 24 h after treatment. If testosterone propionate was given rather than testosterone, the level of LH was significantly reduced (P less than 0.001) 24 h after the injection and the concentration of testosterone in the plasma corresponded to that found in the intact adult male pig. Treatment with oestradiol or oestradiol benzoate did not affect the concentration of LH. Orchidectomy and treatment of pubertal male pigs with testosterone propionate resulted in a significantly (P less than 0.001) higher concentration of testosterone in the plasma, compared with newborn pigs treated similarly, but the level of LH was unchanged. This suggests that there is a more rapid rate of clearance of testosterone in the newborn than in the pubertal male miniature pig and that the negative feedback of testosterone is not mediated by aromatization in the newborn animal and it declines before or during puberty. Treatment of newborn intact male and female and gonadectomized male pigs with oestradiol benzoate produced similar variations in the plasma level of oestradiol in all groups of animals. In the female pigs, however, a surge-like release of LH was observed 60--72 h after the injection of oestradiol benzoate, suggesting that the stimulatory feedback mechanism can operate soon after birth and that the response is sexually dimorphic.

Animals↗