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Biomedical subjects

P Eneroth

Publications and source records attributed to P Eneroth.

At least 271 records · Page 15Linked to original sources
PubMed1981

Rat prolactin and hypothalamic catecholamine nerve terminal systems. Evidence for rapid and discrete increases in dopamine and noradrenaline turnover in the hypophysectomized male rat.

Rat prolactin produces in a dose of 100 micrograms/kg a rapid and marked increase of dopamine turnover in the medial palisade zone of the median eminence and of noradrenaline turnover in the posterior periventricular hypothalamic region as well as a possible minor increase of noradrenaline turnover in the magnocellular part of the paraventricular hypothalamic nucleus of the hypophysectomized male rat. The rat prolactin serum levels measured 2 h following injection were within the upper physiological range of lactating rats. The findings suggest that dopamine in the medial palisade zone may be released as a prolactin inhibitory factor and respond rapidly to increases in serum prolactin levels. Furthermore, rat prolactin can acutely modify noradrenergic mechanisms in discrete areas of the hypothalamus indicating that prolactin can participate in the regulation of types of hypothalamic functions other than regulation of its own secretion.

Animals↗
PubMed1981

Long-term treatment with zimelidine leads to a reduction in 5-hydroxytryptamine neurotransmission within the central nervous system of the mouse and rat.

Male rats and mice received a 14 day peroral treatment with zimelidine, a novel antidepressant drug. Zimelidine produced a 70 and 60% reduction in the number of high affinity [3H]5-hydroxytryptamine (5-HT) and [3H]D-lysergic acid diethylamide (LSD) binding sites, respectively, and induced low affinity binding sites for [3H]5-HT and for [3H]D-LSD. The head twitch behaviour induced by 5-hydroxytryptophan and 5-methoxydimethyltryptamine was attenuated and reductions of prolactin and growth hormone were observed. These findings give further evidence that long-term treatment with zimelidine can produce a reduction of 5-HT neurotransmission in several brain regions.

Animals↗
PubMed1981

The occurrence of immunoglobulin E in Human seminal plasma.

The presence of IgE in human seminal plasma has been explored using two different radioimmunoassay methods. Samples were obtained from 84 patients under investigation for involuntary infertility. Low levels were recorded in seminal plasma (less than 0.05-805 kIU/1) together with a wide scatter of serum values (less than 0.5-956 kIU/1). The incidence of detectable seminal plasma IgE was related to high serum IgE values (P less than 0.001; chi 2-test). Among men reporting allergy problems and who has serum IgE levels above 50 kIU/1 detectable semen IgE was seen in 15 out of 18 patients. Sperm agglutination was observed in 18 men of whom 11 had detectable seminal plasma IgE. The question of whether or not seminal plasma IgE is a plasma transudate or is locally produced as well as its possible function in seminal plasma is discussed.

Female↗
PubMed1981

Nicotine-induced increases of noradrenaline turnover in discrete noradrenaline nerve terminal systems of the hypothalamus and the median eminence of the rat and their relationship to changes in the secretion of adenohypophyseal hormones.

The effects of acute single doses (0.3 and 1 mg/kg) of nicotine on various hypothalamic catecholamine nerve terminal systems and on the secretion of adenohypophyseal hormones in the rat were studied. Nicotine, in a dose of 1.0 mg/kg, increased noradrenaline turnover in the median eminence and in the peri- and paraventricular hypothalamic regions. The dopamine and noradrenaline nerve terminal systems in the median eminence and the dorsomedial hypothalamic nucleus respectively were unaffected. Serum GH levels were decreased and serum prolactin levels increased after a dose of 1 mg/kg. In the presence of tyrosine hydroxylase inhibition, nicotine in a dose of 1 mg/kg, instead increased GH and also LH secretion. It is suggested that the preferential increases of noradrenaline turnover in various hypothalamic noradrenaline nerve terminal systems by nicotine may be partly responsible for the nicotine induced increases of serum prolactin. GH and LH levels observed.

Animals↗
PubMed1981

Continuous infusion of growth hormone feminizes hepatic steroid metabolism in the rat.

The metabolism of 4-[4-14C]androstene-3,17-dione was studied in the microsomal fraction of rat livers after continuous administration of human GH (hGH) in Alzet osmotic minipumps under varying conditions. hGH caused a complete feminization of hepatic steroid metabolism (i.e. increased the 5 alpha-reductase and decreased the 6 beta- and 16 alpha-hydroxylase activities) in normal male rats when infused at a rate of 5 microgram/h for 7 days. Hypophysectomy and castration or adrenalectomy and thyroidectomy of male rats did not reduce the feminizing capacity of hGH, indicating that the adrenals and the thyroid gland are not involved in the mediation of the feminizing effect of hGH. The same dose (5 microgram/h for 7 days) of hGH was also able to refeminize the liver steroid metabolism in hypophysectomized-ovariectomized female rats. The effect of the homologous hormones, rat PRL and rat GH on hepatic steroid metabolism was also investigated. Either hormone was infused at a rate of 10 microgram/h for 7 days, a dose which was sufficient to increase the serum level of the hormone in hypophysectomized animals. No feminizing effect was seen after the administration of rat PRL, whereas rat GH caused a partial feminization of hepatic steroid metabolism in hypophysectomized male animals. It is concluded that GH or a hormone related to GH is involved in sexual differentiation of liver steroid metabolism.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1981

Role of the hypothalamo-pituitary-liver axis in sex differences in susceptibility of the liver to toxic agents.

At birth testicular androgens irreversibly program brain centers involved in hypothalamopituitary control of hepatic sex-dependent steroid and drug metabolism. This imprinting process results in activation of a hypothalamic "feminostatin"-a secreting center that is turned on just before puberty. Feminostatin inhibits pituitary secretion of "feminizing factor," a pituitary hormone that feminizes the basal type of metabolism characterizing the liver of hypophysectomized and gonadectomized rats. Consequently, female rats that are devoid of feminostatin will secrete feminizing factor from the pituitary, leading to a feminine type of hepatic metabolism. Male rats have an active feminostatin-secreting center, and inhibition of pituitary feminizing factor release results in an autonomous type of liver metabolism. Female rats show a relative androgen unresponsiveness and seem incapable of releasing feminostatin after treatment with natural androgens, possibly because of more efficient metabolism (breakdown) of androgen in the female than in the male rat brain. Frontal deafferentation at the retrochiasmatic and suprachiasmatic level resulted in a complete "feminization" of hepatic steroid metabolism in male rats. Such an effect was also seen when lesions involving mainly the anterior periventricular hypothalamic area and the suprachiasmatic nucleus were performed in male rats. No effects were seen in analogous lesions in female rats in any of the cases studied. These findings suggest that a region including the anterior hypothalamic periventricular area, the suprachiasmatic nucleus and adjacent areas is involved in the control of hepatic steroid metabolism. It is postulated that the neuronal cell bodies that produce feminostatin have their origins in this area of the hypothalamus or may send axons through this area to the basal hypothalamus and thus directly or indirectly influence the anterior pituitary gland. Regulation by the central nervous system of a "lactogenic" (prolactin, Prl) receptor, present in the female rat liver, was also studied. This receptor is present in very low concentration or absent in the male rat. Anterior hypothalamic deafferentation at the retrochiasmatic level in male rats increased the hepatic Prl receptor concentration to the female level 3-4 days following the operation. A transection rostral to the suprachiasmatic nucleus had no effect on the concentration of Prl receptors in male animals. Our results demonstrate that the number of Prl receptors is regulated by the hypothalamo-pituitary system. The receptor-inducing pituitary factor might be related to the feminizing factor. Experiments were carried out to elucidate the nature of the Prl receptor-inducing pituitary factor. Human growth hormone (hGH) continuously administered was shown to induce Prl receptors in livers from male and female hypophysectomized-gonadectomized rats. The prolactin receptors were increased to a level found in control female rat livers. This inductive effect of hGH was also seen in adrenalectomized and thyroidectomized male rats. The induced Prl receptors in male rats had similar characteristics as hepatic Prl receptors in female rats. Also the endogenous rat hormones, rPrl and rGH, were administered in minipumps. In the concentration used (10 mug/mul), rPrl had no effect whereas rGH increased Prl receptor levels to approximately 37% of the female control level. These results indicate that GH or a peptide related to GH may be involved in the regulation of hepatic Prl receptors. The hypothalamo-pituitary-liver axis represents a new concept in endocrine regulation of drug toxicity. The male rat liver has been shown to be more susceptible than the female rat liver to the hepatocarcinogenic action of certain drugs, and it is conceivable that sex differences in the metabolic activation of the drugs in the liver may explain the greater sensitivity of male rats to chemically induced hepatocellular carcinoma. Similar sex differences in liver cancer incidence have been reported in the human.

Aging↗
PubMed1981

Serum levels of oestradiol-17 beta and progesterone in relation to sexual receptivity in intact and ovariectomized rats.

Serum levels of oestradiol-17 beta fluctuated markedly during the oestrous cycle or rats. The onset of sexual receptivity occurred in close correlation with increasing serum levels of progesterone. The serum levels of oestradiol and progesterone in ovariectomized rats implanted with constant-release implants filled with oestradiol or progesterone were related to the amount of hormone in the implants. Constant low serum levels of oestradiol stimulated sexual behaviour in ovariectomized rats, but progesterone stimulation was required for maximum behavioural responses. Peak levels of progesterone in the serum during the oestrous cycle were much higher than those needed for induction of the behaviour in ovariectomized, oestradiol-treated rats. Progesterone, administered in physiological doses, inhibited the induction of sexual receptivity caused by oestradiol and progesterone and the inhibition depended on the strength of the stimulation with oestradiol.

Animals↗
PubMed1981

Induction of sexual receptivity in ovariectomized rats by pulse administration of oestradiol-17 beta.

Constant-release implants filled with oestradiol-17 beta induced sexual receptivity in ovariectomized rats in response to progesterone treatment if they were implanted 32 h before behavioural testing. A 20 h period of exposure to oestradiol, by implantation 32 h before testing and removal of the implants 20 h later, was sufficient for induction of the behaviour. The exposure time necessary for behavioural responses could be further reduced to two 4 h periods, between 32 and 28 h and between 16 and 12 h, before testing. Serum levels of oestradiol were raised within 1 h of oestradiol implantation and declined rapidly after implant removal. A single injection of oestradiol benzoate was much more potent than a single injection of oestradiol in inducing sexual receptivity in ovariectomized rats, but this difference in potency was reversed if two appropriately timed injections were given. Oestrone- or oestriol-filled implants were relatively ineffective in inducing sexual receptivity. It is suggested that oestradiol has to be present at crucial time points to prepare an ovariectomized rat to respond behaviourally to progesterone treatment and that oestradiol is the principal oestrogen in the stimulation of sexual behaviour in female rats.

Animals↗
PubMed1981

Evidence that progesterone does not inhibit the induction of sexual receptivity by oestradiol-17 beta in the rat.

Progesterone-filled constant-release implants facilitated the induction of sexual receptivity in ovariectomized rats given implants of oestradiol-17 beta precisely 32 h before testing, irrespective of the time of implantation. Inhibition by progesterone implants of the behavioural response to an injection of progesterone occurred after the facilitation 32 h after oestradiol implantation. Sexual receptivity could be induced in pseudopregnant rats in the absence of progesterone treatment by injection of 1 microgram oestradiol 32 and 16 h before testing at a time when endogenous serum levels of oestradiol were low and progesterone levels were high. The behavioural response of ovariectomized rats implanted with oestradiol and tested daily was unaffected by implantation of progesterone at the time of oestradiol implantation, although serum levels of progesterone varied with the number of progesterone implants inserted. Inhibition by progesterone implants of the behavioural response to an injection of progesterone 6 h before behavioural testing occurred only if the progesterone implants were present for at least 32 h of a 48 h period. Serum levels of progesterone were raised within 1 h of progesterone implantation and declined within a 6 h period after implant removal. It is concluded that progesterone does not inhibit the behavioral effect of oestradiol and that progesterone does not play an inhibitory role in the regulation of the behavioural oestrous cycle in our strain of rats.

Animals↗
PubMed1981

Effects of acute central and peripheral administration of nicotine on ascending dopamine pathways in the male rat brain. Evidence for nicotine induced increases of dopamine turnover in various telencephalic dopamine nerve terminal systems.

The actions of intraventicular injections and intravenous infusions of nicotine were studied on dopamine stores and turnover in discrete areas of the forebrain of normal male rats. This was done by measuring the decline of the dopamine stores after tyrosine hydroxylase inhibition using alpha-methyl-tyrosine methyl ester (H44/68). The dopamine concentrations in the various telencephalic dopamine nerve terminal systems were measured using the Falck-Hillarp methodology involving quantitative microfluorimetry. The catecholamine concentrations in the anteromedial frontal cortex were measured biochemically using high pressure liquid chromatography combined with electrochemical detection. Intraventricular experiments. The dopamine levels in discrete areas of nuc. caudatus and nuc. accumbens were significantly reduced even with the lowest dose of nicotine (1 microgram/rat). Intraventricular injections of nicotine in a dose of 100 microgram/rat produced significant increases of dopamine turnover in various types of dopamine nerve terminal systems in the nuc. caudatus, nuc. accumbens and tuberculum olfactorium, and following a dose of 10 microgram/rat increases of dopamine turnover were observed in the medial part of the nuc. caudatus. Furthermore, nicotine (100 microgram/rat) significantly increased noradrenaline but not dopamine turnover within the anterofrontal cortex. Intravenous experiments. The dopamine levels were selectively reduced by nicotine (1000 microgram/kg) in the cholecystokinin positive and negative dopamine nerve terminal systems of the nuc. accumbens. On the other hand, dopamine levels in the anteromedial frontal cortex were increased after this dose of nicotine. Intravenous infusions of nicotine (10-1000 microgram/kg) produced dose-related increases of dopamine turnover in the various dopamine nerve terminal systems analysed in the telencephalon. These effects became significant with a dose of 1000 microgram/kg/h. The dopamine terminals in the nuc. caudatus showed a higher sensitivity to intravenous infusions of nicotine, being affected by 10-100 microgram/kg of nicotine. These findings suggest that relatively low dose of nicotine via an activation of central nicotine-like cholinergic receptors can reduce dopamine concentration and increase dopamine turnover in discrete limbic and striatal areas. These actions may in part represent the neurochemical basis for the rewarding actions of nicotine and for nicotine dependence in man.

Afferent Pathways↗
PubMed1980

Hypothalamo-pituitary regulation of hepatic prolactin receptors in the rat.

The number of specific binding sites for 125I-labeled human prolactin (hPrl) in crude membrane fractions from rat liver is sexually differentiated. Livers from female rats specifically bound much more of added [125I]hPrl than male liver membrane fractions which bound little, if any, Prl. Hypophysectomy of female animals eliminated hepatic binding of Prl; the effect was reversed by a pituitary implant under the kidney capsule. Treatment of male rats with estradiol valerate induced hepatic hPrl receptors, but only in the presence of an intact pituitary. Anterior hypothalamic deafferentation at the retrochiasmatic level in male rats increased the hepatic hPrl receptor concentration to the female level 3-4 days following the operation. This induction of hPrl receptors was also seen in the absence of the gonads. A transection rostral to the suprachiasmatic nucleus had no effect on the concentration of hPrl receptors in male animals. Our results demonstrate that [125I]hPrl binds specifically to rat liver membranes and that the number of binding sites is regulated by the hypothalamo-pituitary system. The regulatory brain centre appears to be located in the anterior hypothalamus or adjacent areas. The receptor-inducing pituitary factor might possibly be related to the so-called 'feminizing factor' involved in pituitary control of liver enzymes that metabolize drugs and steroids.

Animals↗
PubMed1980

Androgen metabolism in rat anterior pituitary cells in culture.

The metabolism in vitro of 4 androgens, namely testosterone, androstenedione, 5 alpha-dihydrotestosterone and 3 alpha-androstanediol has been studied in male and female rat anterior pituitary cells in primary culture. When testosterone was used as precursor, androstenedione, 5 alpha-dihydrotestosterone and 3 alpha-androstanediol were the main metabolites whereas androstendione was mainly converted into testosterone, 5 alpha-androstanedione, 5 alpha-dihydrotestosterone and androsterone. Studies on the metabolism of 5 alpha-dihydrotestosterone and 3 alpha-androstanediol showed that these compounds were easily interconverted and were also significantly metabolized to 5 alpha-androstanedione and androsterone. No aromatized compounds could be detected suggesting that androgen action in the pituitary cell occurs directly via the androgen receptor rather than through prior conversion into estrogens.

Androgens↗