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Biomedical subjects

R W Steger

Publications and source records attributed to R W Steger.

At least 109 records · Page 6Linked to original sources
PubMed1983

Interactions of delta 9-tetrahydrocannabinol (THC) with hypothalamic neurotransmitters controlling luteinizing hormone and prolactin release.

The effects of delta 9-tetrahydrocannabinol (THC) on hypothalamic norepinephrine (NE) and dopamine (DA) turnover and hypothalamic serotonin (5-HT), 5-hydroxyindole acetic acid (5-HIAA) and LHRH content preceding and during a progesterone- (P) induced LH and prolactin (PRL) surge were investigated in ovariectomized estrogen-primed rats. THC had no effect on basal LH levels, but it inhibited basal PRL levels and blocked the surges of both LH and PRL. The turnover of NE, as estimated by measuring NE depletion after inhibition of tyrosine hydroxylase with alpha-methyl tyrosine (250 mg/kg), in both the anterior (AH) and medial basal hypothalamus (MBH) was significantly inhibited by THC. THC did not significantly affect AH or MBH DA or 5-HT content nor MBH-DA-turnover. Hypothalamic LHRH levels were significantly elevated 4 h after THC administration as compared to the vehicle-injected controls, but pituitary response to exogenous LHRH was not affected. These data suggest that THC inhibits the steroid-induced positive feedback release of LH by reducing NE metabolism and the release of hypothalamic LHRH. Although the mechanism for the inhibition of PRL release by THC is not clear from these experiments, it does not appear that alterations in DA turnover are a contributing factor.

Animals↗
PubMed1983

Dopaminergic stimulation of pituitary but not hypothalamic estrogen receptors in ovariectomized rats.

This study was designed to examine the role of catecholamines and serotonin in the regulation of estrogen receptors (ER) in the medial basal hypothalamus (MBH) and anterior pituitary gland (AP) of adult ovariectomized rats. Plasma PRL and LH were also determined. Injection of alpha-methyl tyrosine (alpha-MT) resulted in the significant reduction of norepinephrine and dopamine (DA) content in the MBH, and of plasma LH levels as well as in the significant elevation of plasma PRL levels. This treatment also resulted in the significant reduction of ER concentration in the AP. The elevation in plasma PRL by alpha-MT was reversed by the simultaneous injection of bromocriptine (BC), a DA agonist, which also partially reversed the alpha-MT reduction of ER concentrations in the AP. BC had no effect on plasma LH levels. The ER concentration in the MBH was not significantly changed by any of these treatments. The reduction of serotonin content in the MBH by the injection of p-chlorophenylalanine had no effect on the ER concentration in either the MBH or AP, nor did it have any effect on plasma PRL levels. However, p-chlorophenylalanine treatment did decrease plasma LH levels. Neonatal treatment of female rats with monosodium glutamate which has been reported to destroy part of the MBH, resulted in a significant reduction in body and pituitary weight and in a significant elevation of plasma PRL levels in adults (2 months old). This treatment also resulted in a significant reduction in the AP and MBH ER concentration. Injection of BC to adults reversed the effects of neonatal monosodium glutamate treatment on plasma PRL levels and on the pituitary ER concentration, but had no effect on the ER concentration in the MBH. BC had no effect on the AP or MBH ER concentration in control rats, although it did as expected reduce the plasma PRL levels in these animals. Plasma LH levels were not significantly changed by any of these treatments. Injection of the DA antagonist, haloperidol, to adult rats resulted in a significant elevation of plasma PRL and in a significant reduction of ER concentration in the AP. Haloperidol treatment did not affect the binding affinity of these receptors. Overall, these data suggest that DA is involved with the regulation of ER in the AP.

Animals↗
PubMed1983

The effects of photoperiod on the responses of the hamster vas deferens to nerve stimulation.

Hamster vas deferens responds to nerve stimulation with a biphasic contraction which is completely blocked by guanethidine and tetrodotoxin. The second component of the contraction is inhibited by phentolamine, whereas the initial component is slightly potentiated by phentolamine. When hamsters are subjected to short photoperiods or castration, the vas deferens becomes supersensitive to nerve stimulation and shows spontaneous mechanical activity. The supersensitivity is not due to increased postsynaptic adrenergic supersensitivity, decreased neuronal uptake of catecholamine, decreased presynaptic feedback by prostaglandin or adrenergic agonist. The supersensitivity is still demonstrable in the presence of 4-aminopyridine, suggesting that the release of transmitter is also not different in animals kept in short photoperiods. The activity of the Na+/K+ pump is increased in vasa deferentia from hamsters kept in short photoperiods and the postsynaptic response to the ATP receptor agonist, diadenosine pentaphosphate, is also enhanced. It is suggested that the supersensitivity induced in the hamster vas deferens by short photoperiod is caused by testosterone withdrawal and is due to increased responsiveness to ATP, which could be acting as a cotransmitter in this tissue.

Animals↗
PubMed1982

Alterations in neuroendocrine function during photoperiod induced testicular atrophy and recrudescence in the golden hamster.

Transfer of golden (Syrian) hamsters from a 14L:10D (Light:dark) to a 5L:19D photoperiod causes profound changes in the reproductive axis. Testicular weight fell within 7 weeks of short photoperiod exposure and remained low until 19 weeks, at which time spontaneous recrudescence began. Plasma LH, FSH, and Prl levels were undetectable at 7.5 weeks of exposure, but LH and FSH returned to basal levels by 15 weeks and Prl by 20.5 weeks. Hypothalamic LHRH levels increased concurrently with the fall in LH and FSH, suggesting that LHRH release was decreased. Increasing plasma gonadotropin levels and testicular recrudescence were associated with decreases in hypothalamic LHRH content. Hypothalamic norepinephrine (NE) turnover was low at 10 weeks, suggesting that decreased LH and FSH levels were ultimately due to decreased adrenergic activity. At 15 weeks, plasma LH levels and hypothalamic NE turnover were both increased over values seen at 10 weeks. Hypothalamic dopamine turnover, possibly reflecting decreased Prl feedback, was decreased between 0 and 10 weeks, but returned to control level by 15 weeks. It, therefore, appears that the endocrine changes associated with photoperiod induced testicular regression and recrudescence are secondary to changes in hypothalamic function.

Animals↗
PubMed1982

Failure of indomethacin to block the estrogen-induced luteinizing hormone surge in the ovariectomized rhesus monkey.

Prostaglandins have been shown to be stimulatory to LH release in several species, although it is not known, in the primate, whether this effect is mediated through the hypothalamic-pituitary axis or by an indirect effect mediated through the ovary. In the present experiments, indomethacin, an inhibitor of prostaglandin synthesis, did not significantly alter basal LH levels or the positive and negative feedback effects of estrogen on LH release in the ovariectomized rhesus monkey. Therefore, it appears that the previously demonstrated effect of indomethacin on LH release in the intact monkey was mediated through ovarian mechanisms.

Animals↗
PubMed1982

A quantitative difference between immunologically and biologically active prolactin in hypothyroid patients.

Under certain conditions, the pituitary may secrete PRL species displaying diverse immunological and biological activities. To study this phenomenon further, we compared PRL determined by RIA and radioreceptor assay (RRA) in 25 hypothyroid patients (TSH, greater than 10 microU/ml) and in 49 endocrinologically normal patients. In the normal women, the ratio of the PRL mean determined by RRA (67.3 ng/ml) to that determined by RIA (13.5 ng/ml) was 4.99 +/- 0.435. By contrast, in hypothyroid patients, PRL determined by RRA was significantly lower than the value determined by RIA for each patient, and the ratio of means (RRA to RIA) was 0.782 +/- 0.067. The mean PRL determined by RRA (52.2 ng/ml) was not significantly different from the mean of control patients (P greater than 0.5). PRL determined by RIA was elevated in all hypothyroid patients (range, 24-237 ng/ml), and the mean (by RIA) (64.1 ng/ml) was significantly elevated above the mean PRL (by RIA) of controls (P less than 0.000001). Thus, in the chronically hypothyroid patients, PRL is characterized as possessing normal receptor-binding activity and augmented immunological activity.

Adult↗
PubMed1982

Interaction between pargyline, a monoamine oxidase inhibitor, and beta-adrenergic receptors in the rat pineal gland.

The hypothesis that pargyline, a monoamine oxidase inhibitor, may interact with pineal beta-adrenergic receptors to increase N-acetyltransferase (NAT) activity and, thereby, melatonin content was tested in intact and superior cervical ganglionectomized (SCGX) rats some of which were also treated with the tryptophan hydroxylase inhibitor para-chlorophenylalanine (PCPA). Pargyline injection increased both NAT activity and melatonin content, an effect nullified by conjunct propranolol injection. While pargyline injection also increased NAT activity in intact, PCPA-treated rats, the effects of this drug were most evident in SCGX, PCPA-treated rats. PCPA treatment prevented pargyline-induced increases in melatonin content in intact and SCGX rats suggesting an artificially-induced dissociation of melatonin biosynthesis from its rate-limiting enzyme. We suggest that pargyline may be capable of interacting with pineal beta-adrenergic receptors to increase NAT activity in the absence of pineal norepinephrine (NE) and serotonin.

Animals↗
PubMed1981

Age related changes in the control of prolactin secretion in the female rat.

The purpose of this investigation was to evaluate the effects of advancing age on the control of pituitary prolactin secretion. The effects of dopaminergic inhibition and estrogen stimulation of pituitary prolactin secretion were tested both in vivo and in vitro. Estrogen stimulated prolactin secretion in both old and young animals, and elevated estrogen levels in old rats may be partially responsible for elevated prolactin levels. Oral L-DOPA administration induced cycles in old rats but had no effect on prolactin levels in either old or young rats. Injections of L-DOPA lowered prolactin in young but not in old rats, while apomorphine reduced prolactin levels in both groups. The pituitaries of young rats secrete more prolactin in vitro than old pituitaries, further supporting a decrease in hypothalamic DA turnover as a cause for elevated prolactin levels in old rats.

Aging↗
PubMed1981

Effects of CNS active drugs and somatostatin antiserum on growth hormone release in young and old male rats.

The capacity of several potent pharmacological agents to increase growth hormone (GH) release was tested in young (3- to 4-month-old) and old (18- to 20-month-old) male Sprague-Dawley rats. Young and old animals were injected with alpha-methyl-p-tyrosine (250 mg/kg), a catecholamine synthesis inhibitor, followed 60 min later by the alpha-adrenergic receptor agonist, clonidine hydrochloride (150 micrograms/kg). Plasma GH levels increased to greater than 276 ng/ml by 30 and 50 min in young rats, whereas values never exceeded 130 ng/ml (p less than 0.01) in old rats. Piribedil methane sulfonate (1 mg/kg), a dopamine receptor agonist, significantly increased GH in young animals 60 min after injection (p less than 0.01), but had no effect in old rats. Morphine sulfate (5mg/kg) increased plasma GH concentration in young rats to greater than 400 ng/ml at 30, 50 and 70 min after injections, whereas values in old animals never exceeded 300 ng/ml (p less than 0.01). 15 min after injection of somatostatin antiserum No. 774 (5 ml/kg), plasma GH levels increased to greater than 750 ng/ml in both young and old rats. Administration of greater volumes of somatostatin antiserum (8 ml/kg) increased GH levels more in old than in young animals 30 and 45 min after injection (p less than 0.01). These results indicate that old male rats have less capacity to increase GH in response to agents that normally enhance GH release. This may be the result of a diminished number of affinity of post-synaptic neurotransmitter receptors, or to an increased release of somatostatin. Since somatostatin antiserum in creased H equally or to a greater extent on old that in young animals, aging rats may release more somatostatin or the pituitary may be more sensitive to the inhibitory effects of this hormone.

Aging↗
PubMed1981

Glucocorticoid suppression of pituitary prolactin release in the nonhuman primate.

The administration of 8 mg dexamethasone daily for 8 days significantly lowered basal and TRH-stimulated PRL levels in ovariectomized rhesus monkeys. A single acute injection of dexamethasone attenuated the total amount of PRL released after TRH stimulation, although basal and peak PRL levels were not significantly different from those found in controls. In an attempt to determine the site of action of glucocorticoids on PRL secretion, baboon pituitaries were incubated with cortisol. Cortisol at a concentration of 3 x 10(-5) M significantly inhibited PRL secretion in vitro, while a concentration of 3 x 10(-4) M was needed to block TRH-stimulated prolactin release. In conclusion, glucocorticoids can suppress pituitary PRL secretion by a direct action on the pituitary gland, although a hypothalamic site of action may also be involved.

Animals↗
PubMed1981

Interactions of cocaine and delta 9-tetrahydrocannabinol with the hypothalamic-hypophysial axis of the female rat.

The acute effects of cocaine and/or delta 9-tetrahydrocannabinol (THC) were studied in ovariectomized female rats. Intermediate doses of cocaine (10 or 20 mg/kg) caused an increase in serum luteinizing hormone (LH) and a decrease in serum prolactin levels, whereas a higher dose (40 mg/kg) caused a decrease in serum LH. THC (10 mg/kg) attenuated serum LH and prolactin levels. The THC effect on LH was blocked by cocaine. Neither drug alone or in combination affected serum follicle-stimulating hormone levels. The cocaine-induced changes in LH levels were closely paralleled by changes in hypothalamic norepinephrine content, suggesting a neurochemical basis for cocaine's action on LH release.

Animals↗
PubMed1980

Ultrastructural alterations associated with the initiation of follicular atresia.

To identify and describe ovarian follicles committed to undergo follicular degeneration (atresia), immature rats were primed with pregnant mare serum gonadotropin (PMSG). After PMSG treatment, preovulatory follicles develop but subsequently degenerate. Prior to the appearance of pyknotic nuclei (Stage I of atresia), degenerative changes were observed in focal areas of the granulosa cell layer. These changes include "blebbing" of the cytoplasm and alterations in the shape of the granulosa cells. The appearance of these degenerative changes coincides with a decrease in ovarian concentrations of estradiol and testosterone. Since estrogens and androgens maintain the follicle, the decline in estradiol and testosterone could be responsible for the further degenerative alterations that lead to complete deterioration of the preovulatory follicle. In Stage I atretic follicles, lysosome-derived autophagic vacuoles develop and macrophages invade both the thecal and granulosa cell layers. The combined actions of the autophagic vacuoles and macrophages could destroy both the granulosa-cell and thecal layers and thereby transform the preovulatory follicle into an ovarian cyst.

Animals↗
PubMed1980

Effects of PGF2 alpha-induced luteolysis and progesterone on follicular growth in pregnant mice.

The effects of a luteolytic dose of prostaglandin F2 alpha on follicular development within the ovary of pregnant mice were studied in vivo and in vitro. The results showed that 1) PGF2 alpha reduced the number of growing primary follicles both in vivo and in vitro, 2) in vitro, progesterone and LH/FSH override this effect of PGF2 alpha and 3) progesterone suppresses the rate at which primary and preantral follicles grow. It is concluded that in the ovary of the pregnant mouse, progesterone regulates the number of primary follicles which start to grow; while gonadotropins and intraovarian progesterone levels control the rate at which primary and preantral follicles develop.

Animals↗
PubMed1980

Capacity of old versus young male rats to release thyrotropin (TSH), thyroxine (T4) and triiodothyronine (T3) in response to different stimuli.

Serum TSH, T4 and T3 were measured by radioimmunoassay (RIA) in 20-24 month old and 6-8 month old Long-Evans male rats during basal conditions, and upon exposure to cold temperature (4 degrees C), injection of ovine TSH, thyroidectomy, and T4 or T3 treatment. Basal serum TSH values in the old and young rats were similar, but serum T4 and T3 levels in the old rats were significantly lower than in the young rats. No differences were observed in TSH release between old and young rats in response to cold temperature, but old rats whowed no rise in serum T4, TSH administration produced a significantly smaller increase in serum T4 in old rats, but similar increases in serum T3 in old and young rats. No differences were observed between old and young rats in the rise of serum TSH after thyroidectomy, or in the fall of serum TSH after T4 or T3 administration. These results are believed to indicate that the primary cause for reduced thyroid function in old rats lies in the thyroid gland itself.

Aging↗