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Biomedical subjects

E Düker

Publications and source records attributed to E Düker.

7 recordsLinked to original sources
PubMed1988

Pituitary-dependent effects of estradiol-17-beta on catecholamine turnover rates, gamma-aminobutyric acid and glutamate concentrations in various hypothalamic and limbic brain structures.

Estrogens exert many effects in a variety of hypothalamic and mesolimbic structures. Whether the actions of the estrogens are direct or indirect, possibly involving anterior pituitary hormones, is largely unknown. We therefore studied catecholamine turnover rates, gamma-aminobutyric acid and glutamate concentrations in various hypothalamic and mesolimbic structures in estrogen-treated hypophysectomized (hypox) rats and compared the measured parameters with those in sham hypophysectomized (sham) animals. Results clearly demonstrate that many of the effects of estrogen require an intact pituitary. Dopamine turnover rates in hypox rats were significantly reduced in the hypothalamus and the striatum, whereas they increased in the medial septum and medial preoptic area in comparison with sham rats. Norepinephrine turnover rates were reduced in the anterior mediobasal hypothalamus, somatosensory cortex and the nucleus accumbens of hypox animals in comparison with the sham-operated animals. In contrast, norepinephrine turnover was accelerated in the mediocortical amygdala and posterior medial basal hypothalamus of hypox rats. A significant reduction of epinephrine turnover was evident in the nucleus accumbens of hypox rats. Gamma-aminobutyric acid concentrations increased in the medial septum, anterior and posterior part of the mediobasal hypothalamus, but decreased in the mediocortical amygdala of hypox animals. Concentrations of glutamate were also decreased in the mediocortical amygdala in hypox animals. These results indicate that many direct effects of estrogens in the brain are accompanied by indirect effects which require an intact pituitary.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Effects of systemic and local administration of etomidate on adrenocortical steroidogenesis in male rats.

A method for focal dialysis of the adrenal cortex is introduced allowing determination of adrenal steroid local release rates in conscious, freely moving rats. Etomidate, an anaesthetic drug known to interfere with adrenal steroid synthesis, blocks not only corticosterone but also aldosterone and, to a lesser degree, progesterone release. Intra-adrenal application of the drug via the dialysis system for a defined time resulted in low release rates of corticosterone without inducing sedation of the animals or even anaesthesia. Remaining low steroid concentrations during the next 5 h after cessation of the dialysis with drug-containing medium indicate that the inhibition of steroid synthesis lasted for several hours. It is concluded that the inhibitory effect of etomidate on steroid biosynthesis can be explained on the basis of an interaction of the drug with adrenocortical enzymes without the involvement of hypothalamic or hypophyseal mechanisms.

Adrenal Cortex↗
PubMed1984

In vivo release of neurotransmitters in the medial basal hypothalamus of the monkey.

In vivo release rates of norepinephrine (NE), epinephrine (E), dopamine (DA), gamma-aminobutyric acid (GABA), glutamate (GLU) and beta-endorphin (beta E) in the medial basal hypothalamus (MBH) of unanaesthetized female macaca fascicularis monkey, and the effects thereon of estrogen (E2) treatment, have been estimated using push-pull perfusion methodology. DA, NE, E, GABA, GLU and beta E were all detectable in 30 min perfusate fractions. No direct correlation between their release rates and those of LH and PRL could be observed. E2 induced an initial decrease, then an increase, in LH and PRL secretion, and concomitant changes in the release patterns of DA, NE, E. GABA and GLU were apparent. This study demonstrates that in vivo push-pull perfusion methodology may be applied to the unanaesthetized monkey, and when combined with venous catheterization for serial blood sampling may prove to be a powerful tool in the investigation of the central molecular events governing neuroendocrine functions.

Animals↗
PubMed1983

Hypothalamic and limbic GABA concentrations and turnover rates and glutamate concentrations following induction of hyperprolactinemia in ovariectomized rats.

Hyperprolactinemia was induced by transplantation of pituitaries of donor rats under the kidney capsule of ovariectomized recipient rats. This results in a permanently increased serum prolactin and temporarily suppressed luteinizing hormone (LH) levels. Concentrations of gamma-aminobutyric acid (GABA) and glutamate as well as turnover rates of GABA were determined in micropunches of the nucleus accumbens (ACB), medial preoptic area (MPO), anterior and posterior part of the mediobasal hypothalamus (AMBH and PMBH) and in the mediocortical amygdala (AMY). GABA concentration in the ACB and MPO were reduced in hyperprolactinemic rats. This was significant at day 8. At days 4 to 21 following pituitary transplantation glutamate concentrations were also significantly reduced in the AMY. The most conspicuous changes in GABA turnover rates were observed in the ACB and MPO. In the former structure hyperprolactinemia reduced GABA turnover, while in the latter high prolactin levels increased GABA turnover at day 4. It is concluded that the suppressive effect of hyperprolactinemia on blood LH levels may involve a preoptic GABAergic component and possibly a glutamatergic mechanism in the AMY. Alternatively, the AMY and the ACB may be involved in eliciting the many behavioral effects associated with hyperprolactinemia.

Animals↗
PubMed1983

Dopamine-inhibited release of prolactin and intermediate lobe-POMC-peptides: different modulation by opioids.

Primary monolayer cultures of anterior or intermediate lobe (IL) cells from rat pituitaries were grown in microtiter plates, and the test substances were added after 5 days. The hormones were measured by RIAs for rat prolactin, -MSH, ACTH and beta-endorphin/beta-LPH. The dopamine (DA) inhibition of prolactin secretion was attenuated by addition of equimolar (10(-7), 10(-6)M) concentration of beta-endorphin. Furthermore, the DA effect was blocked, when the beta-endorphin-release of anterior pituitary cells was stimulated by vasopressin. In contrast, the DA induced inhibition of hormone-release of IL-cells (e.g. -MSH, ACTH and beta-endorphin) was not influenced by addition of opioids. Our results indicate, that under certain conditions (e.g. stress) the stimulated secretion of prolactin could be mediated partially by a direct action of pituitary beta-endorphin at the lactotroph. On the other hand, we found no indication for a modulation of the dopamine-induced inhibition of IL-peptides by opioids.

Adrenocorticotropic Hormone↗