|
11. |
Dopaminergic Regulation of Brain Gonadotropin-Releasing Hormone in Male Goldfish during Spawning Behavior |
|
Neuroendocrinology,
Volume 52,
Issue 3,
1990,
Page 276-283
Liu Yu,
Richard E. Peter,
Preview
|
PDF (1650KB)
|
|
摘要:
Dopaminergic regulation of gonadotropin-releasing hormone (GnRH) concentrations in discrete brain areas of male goldfish was studied using the centrally active dopaminergic agonist apomorphine and antagonist pimozide. Pimozide caused time- and dose-dependent increases in serum gonadotropin levels and accumulation of GnRH in the olfactory bulbs, telencephalon and pituitary. The effects of pimozide were partially antagonized by apomorphine, which, when given alone, did not influence basal levels of brain GnRH and serum gonadotropin, but inhibited the increases in brain GnRH and serum gonadotropin levels that normally occur in response to spawning stimuli from prostaglandin-treated females. To study the physiological significance of the accumulation of brain GnRH due to central dopaminergic receptor blockade, the influences of pimozide on the brain GnRH and serum gonadotropin responses of male goldfish to spawning stimuli were tested. Pimozide pretreatment potentiated the serum gonadotropin increases and caused a marked reduction in the GnRH levels in olfactory bulbs, telencephalon and pituitary in response to spawning stimuli. These findings demonstrate that the central dopaminergic system is an important inhibitory component in the regulatory circuitry of brain GnRH levels in normal and behaviorally stimulated male goldfish.
ISSN:0028-3835
DOI:10.1159/000125598
出版商:S. Karger AG
年代:1990
数据来源: Karger
|
12. |
Decreased Pituitary Growth Hormone Response to Growth Hormone-Releasing Factor in Cafeteria-Fed Rats: Dietary and Obesity Effects |
|
Neuroendocrinology,
Volume 52,
Issue 3,
1990,
Page 284-290
Geneviève Renier,
Pierrette Gaudreau,
Habiba Hajjad,
Nathalie Deslauriers,
Michèle Houde-Nadeau,
Paul Brazeau,
Preview
|
PDF (1314KB)
|
|
摘要:
The in vivo and in vitro growth hormone (GH) responsiveness to growth hormone-releasing factor [rGRF(l-29)NH2] was evaluated in a dietary obese rat model. Sprague-Dawley rats were divided into two groups after weaning. The control group received a semisynthetic defined diet, and the cafeteria-fed group was maintained on a mixed energy-rich palatable diet. After 2 months of diet, the cafeteria-fed rats were divided into two groups, according to their degree of weight gain compared to controls: group I: 0%; group II: 24%. After 5 months of diet, the weight increase was, respectively, in groups I and II, 12 and 41%, as compared to controls. Under pentobarbital anesthesia, rGRF(l-29)NH2 was injected intravenously in two consecutive doses of 0.8 and 4.0 µg/kg body weight into the control and cafeteria-fed rats. After 2 months of diet, a significant decrease of basal GH levels and GH peak response to the 4.0 µg/kg rGRF dose was observed in both cafeteria-fed rat groups as compared to the control group. After 5 months of diet, basal GH levels decreased in both cafeteria-fed groups. However, a significantly blunted GH response to both doses of rGRF occurred only in group II. After 5 months of diet, perifused anterior pituitary cells of control and cafeteria-fed rats were challenged with increasing concentrations of rGRF (6.25, 25 and 100 pM). The basal GH secretion was similar in all groups but the stimulated GH release in response to 25 and 100 pM GRF, expressed as peak value, was depressed in group II, compared to controls. Epididymal fat pad weights were significantly increased in group II 5-month-old rats, compared to controls (p < 0.05). A positive linear correlation was found between fat pad weight and body weight (r = 0.68, p < 0.01). In addition, the peak GH response to 4.0 µg/kg body weight of rGRF was inversely correlated with the total body weight (r = –0.57, p < 0.05) and the fat pad weight (r = –0.71 p < 0.02) in all the cafeteria-fed rats. These data demonstrate an in vivo decreased basal and stimulated GH response to rGRF and an alteration of the GH-stimulated release at the pituitary level in an obese cafeteria rat model and suggest that obesity and/or a cafeteria diet blunts the GH re
ISSN:0028-3835
DOI:10.1159/000125599
出版商:S. Karger AG
年代:1990
数据来源: Karger
|
13. |
Tryptophan Administration Inhibits Nocturnal N-Acetyltransferase Activity and Melatonin Content in the Rat Pineal Gland |
|
Neuroendocrinology,
Volume 52,
Issue 3,
1990,
Page 291-296
Russel J. Reiter,
Thomas S. King,
Stephan Steinlechner,
Richard W. Steger,
Bruce A. Richardson,
Preview
|
PDF (1179KB)
|
|
摘要:
In the rat pineal gland, the activity of serotonin N-acetyltransferase (NAT) and the concentration of melatonin are normally high at night; conversely, the concentration of serotonin (5-HT), the precursor of melatonin, is low. Since tryptophan administration increases the concentration of pineal 5-HT at night, we examined its effect of melatonin production. Nighttime tryptophan loading led to substantial increases in pineal 5-hydroxytryptophan, 5-hydroxyindole acetic acid (5-HIAA), and 5-HT but a highly significant reduction in NAT activity in comparison to saline-injected controls. In contrast to other measured indoles, melatonin levels also were significantly diminished by tryptophan loading. Nocturnally high pineal norepinephrine levels were unaltered by tryptophan administration. The idea that high concentrations of 5-HT could lead to substrate inhibition of NAT activity was not supported by kinetic analysis of control NAT levels versus tryptophan-inhibited NAT activity under varied substrate concentrations. Hypotheses to explain these results include the possibility that tryptophan inhibition of melatonin synthesis is mediated by the release of 5-HT from the pinealocyte and its subsequent autocrine action on melatonin production.
ISSN:0028-3835
DOI:10.1159/000125600
出版商:S. Karger AG
年代:1990
数据来源: Karger
|
14. |
Proopiomelanocortin Messenger RNA Levels Are Increased in the Anterior Pituitary of the Sheep Fetus after Adrenalectomy in Late Gestation |
|
Neuroendocrinology,
Volume 52,
Issue 3,
1990,
Page 297-302
I. Caroline McMillen,
Giuliana C. Antolovich,
Julie E. Mercer,
Roslyn A. Perry,
Marian Silver,
Preview
|
PDF (1259KB)
|
|
摘要:
We have investigated the effect of bilateral adrenalectomy at 116–119 days’ gestation on the levels of the messenger (m) RNA for proopiomelanocortin (POMC) in the anterior pituitary of the fetal sheep and in the ovine placentome during late gestation (134–136 days’ gestation). After fetal adrenalectomy there was a significant (p < 0.001) and sustained increase in circulating ACTH concentrations in the adrenalectomised group (1,838 ± 155 ng/l at 130–136 days) when compared with the intact control group (131 ± 25 ng/l at 130–136 days). The mean levels of POMCmRNA relative to 18S RNA were also significantly higher (p < 0.001) in the adrenalectomised fetal sheep pituitaries (2.8 ± 0.12; n = 4) than in the intact/control fetal sheep pituitaries (1.31 ± 0.13; n = 4). In contrast to the findings in the anterior pituitary, POMCmRNA was not detected in RNA extracted from the placentomes of either the adrenalectomised or intact fetal sheep. There was also a significant arteriovenous difference in ACTH concentrations in the umbilical circulation in both adrenalectomised and intact fetal sheep at 134–136 days’ gestation. This study demonstrates therefore that the fetal adrenals act to suppress POMCmRNA levels in late gestation and also that the increase in circulating ACTH after adrenalectomy originates from the pituitary and
ISSN:0028-3835
DOI:10.1159/000125601
出版商:S. Karger AG
年代:1990
数据来源: Karger
|
15. |
Opiate-Thyroid Hormone Interactions in the Regulation of Thyrotropin Secretion in the Rat |
|
Neuroendocrinology,
Volume 52,
Issue 3,
1990,
Page 303-308
Ann Berglund,
William J. Millard,
Steve M. Gabriel,
James W. Simpkins,
Preview
|
PDF (1083KB)
|
|
摘要:
Studies were performed to determine the role of thyroid hormone in the suppression of thyrotropin (TSH) by opiates. Serum samples were collected by decapitation 1, 3, 6, 12, 24, or 48 h after rats were implanted with 1 sustained-release morphine (75 mg) or placebo pellet. Morphine decreased TSH by 44% at 1 h and by 83% at 3 h, and TSH remained significantly depressed by 38% through 48 h. Thyroxine (T4) levels were significantly reduced from 12 to 24 h after morphine, but triiodothyronine (T3) levels were not affected. When control or thyroidectomized (THX) rats were implanted with morphine or placebo 24 h before serum collection, morphine significantly decreased TSH, T3 and T4 in controls but had no effect on TSH in THX rats. Thus, it appears that the morphine-induced suppression of TSH release requires circulating thyroid hormone. When THX rats were chronically treated with morphine or placebo, then injected subcutaneously with saline or 1, 10 or 100 µg Tt/kg body weight 24 h prior to serum collection, morphine treatment alone did not affect TSH in THX rats. T4 replacement caused a dose-dependent decrease in serum TSH in both morphine and placebo rats; however, TSH was suppressed significantly more in morphine than in placebo rats. Thus, while chronic morphine treatment is ineffective in suppressing in TSH in THX rats, morphine interacts with thyroid hormone to reduce TSH release. These data suggest that morphine may exert its inhibitory effect on TSH secretion by increasing the negative feedback sensitivity to thyroid hormones
ISSN:0028-3835
DOI:10.1159/000125602
出版商:S. Karger AG
年代:1990
数据来源: Karger
|
|