摘要:

The capacity of the fetal pituitary-thyroid system to respond to synthetic TRH (pyroGlu-His-ProNH2) was tested by administration of the hypothalamic hormone on the last day of gestation to intact and hypophysectomized pregnant rats whose thyroids were labeled with 131I 24 h previously. Significant decrease in the ratios of thyroid-blood radioactivity occurred in newborn of TRH-treated mothers. Consistent reduction (30–70 %) in thyroidal 131I uptake and increase in blood radioactivity (12–60%) were observed. Bioassays (stasis tadpole) revealed significant elevation in plasma TSH levels and reduced hormone content of the pituitary in pups of mothers receiving TRH. In utero injections of the hypothalamic hormone into fetuses produced a similar pattern of TSH change within 15 min. Sufficient TSH release occurred to induce histologic activation in the thyroids of spontaneously delivered offspring. The effect of TRH on TSH release by the fetal hypophysis appeared to be specific. No indication of any substantial influence on maternal and fetal pituitary-adrenal system was obser

ISSN:0028-3835    

DOI:10.1159/000122050

出版商:S. Karger AG    

年代:1972

数据来源: Karger

摘要:

Experiments were carried out to elucidate the influence of stress on the diurnal change in adrenal biosynthetic activity during controlled 24 h light-dark cycles. stress Groups of 10 rabbits were decapitated at 3 h intervals and the adrenal glands were rapidly removed for measurement of incorporation of 14C-l-acetate into corticosterone and 17-hydroxycorticosterone in their homogenates. Immobilization stress was applied for 6 h a day. The influence of repeated stress was studied in the rabbits after exposure to 7 immobilization stresses. A diurnal rhythm was observed in the activity of adrenocorticoid biosynthesis in non-stressed rabbits, with a maximum at 18:00 and a minimum at midnight. When the animals were exposed to 6 h of immobilization, the adrenocortical biosynthetic activity showed an 80 % increase at 3 h and a 40 % increase at 6 h; the normal rhythmicity was thus disturbed by exposure to this stressor. The lowest level was observed at 9:00 on the next morning, with a 9 h delay. Where rabbits were repeatedly exposed to immobilization for 7 days, the 7th immobilization did not affect the diurnal rhythmicity of adrenal biosynthetic activity or induce its facilitation.

ISSN:0028-3835    

DOI:10.1159/000122051

出版商:S. Karger AG    

年代:1972

数据来源: Karger

摘要:

Electrical activity in the hypothalamus was recorded following dexamethasone administration to intact and diencephalic-island animals. In intact animals, dexamethasone produced an equal number of increases or decreases in unit resting firing frequencies. At least half of these rate changes were accompanied by alterations in EEG. Of the units tested in the basal hypothalamus of diencephalic-island animals, 50 % were inhibited by dexamethasone within a 10–15 minute period, 9% showed an increased firing rate, and the remainder were unresponsive. The results indicate a direct effect of the hormone on neurons in the isolated basal hypothalamus. Hypothalamic electrical activity was also recorded following the administration of vasopressin and histamine, two agents known to activate the adrenocortical system. The compounds uniformly produced rapid inhibition in unit firing in both intact and diencephalic-island animals. Thus, compounds with opposite actions on ACTH secretion, i.e., dexamethasone or vasopressin and histamine, produce the same inhibitory effect on the firing rate of hypothalamic neuron

ISSN:0028-3835    

DOI:10.1159/000122052

出版商:S. Karger AG    

年代:1972

数据来源: Karger

摘要:

The ovarian compensatory hypertrophy (OCH) response was evaluated in adult female rats bearing bilateral electrolytic lesions in the cortical nucleus of the amygdala (ACO), the stria terminalis (ST), and the cerebral cortex (CCx). The left ovary was removed and weighed at the time of lesioning; 10 days later, the right ovary was removed, weighed, and the percentage increase in weight calculated. There was no difference between the OCH response in non-lesioned controls and that in sham ACO-, or ST-lesioned animals (electrodes lowered but no current passed), nor between the response in rats with CCx lesions and that in the sham controls. In contrast, a significant inhibition of the OCH response was noted in those animals bearing lesions in the ACO or ST when compared to their respective controls. These data indicate that the cortical nucleus of the amygdala plays a critical role in the response of the neuroendocrine network to steroid withdrawal. Further physiological support is also offered for the ST as a vital information link between the amygdala and hypothalamus.

ISSN:0028-3835    

DOI:10.1159/000122053

出版商:S. Karger AG    

年代:1972

数据来源: Karger

摘要:

Previous studies showed suppression of non-stress pituitary-adrenal function 2 h after exposure to physiological levels of plasma corticosterone. To study the latency of such suppression, adult female rats were killed at intervals after receiving 1 mg/kg corticosterone or vehicle s.c. at 14:30. Plasma and adrenal concentrations of corticosterone, measured fluorometrically, were used as indices of magnitude of feedback signal and level of ACTH secretion, respectively. Plasma steroid levels reached a peak of approximately 150 µg/100 ml 5 min after corticosterone injection and by 30 min were declining and approaching those of vehicle-injected controls. Concurrently, corticosterone levels in adrenals fell to basal levels by 30 min after corticosterone injection. In attempts to find the minimum feedback-active dose of corticosterone, interference associated with the estrous cycle was encountered. At 30 min after injection of 0.5 mg/kg corticosterone, adrenal steroid levels in diestrous rats were lower than those of rats in estrus. Injection of 0.5 mg/kg corticosterone in diestrous rats resulted in peak plasma levels of 90 µg/100 ml at 5 min and a return to control levels by 30 min. At 30 min after corticosterone, adrenal levels were totally suppressed. These findings suggest that transient feedback signals within the physiological range may cause rapid and complete suppression of non-stress pituitary-adrenal function in the ra

ISSN:0028-3835    

DOI:10.1159/000122054

出版商:S. Karger AG    

年代:1972

数据来源: Karger

摘要:

Neurosecretory activity of the hypothalamic magnocellular supraoptic and paraventricular nuclei (SON and PVN) was determined in pinealectomized and control young adult female rats subjected to a 12/12 h light rhythm, to continuous light, or to ovariectomy. The distribution of thiamine diphosphate-phosphohydrolase (TPP-ase), an enzyme specific for the Golgi apparatus, was used as a parameter for neurosecretory activity. In both the SON and the PVN, a decrease in neurosecretory activity was observed after pinealectomy, irrespective of additional experimental conditions. The significance of this finding is discussed, especially in regard to a possible general influence of the pineal gland on the neurosecretory nuclei.

ISSN:0028-3835    

DOI:10.1159/000122055

出版商:S. Karger AG    

年代:1972

数据来源: Karger

摘要:

After the injection of 14C-labeled TRH into normal male rats, radioactivity disappeared rapidly from the circulation. The half life of 14C-TRH was found to be 4.16 min; however, the true half life of TRH may be masked, since TRH is rapidly inactivated in the blood to compounds having similar chemical structures and probably similar half lives. Chromatography of methanol extracts of plasma samples taken at 1, 2, and 6 min revealed that some of the radioactivity had the same Rf value as that of TRH, while other areas corresponded to the free acid of TRH (pyro-glu-his-pro-OH), glu-his-pro, and his-pro-NH2. The mean volume of distribution of TRH in our studies was 18.5% of the body weight. Approximately 25% of the radioactivity was excreted into the urine within 60 min after the intravenous injection of 1 µCi of 14C-TRH. Urinary radioactive metabolites appeared to have the same electrophoretic mobilities as TRH and the free acid of TRH

ISSN:0028-3835    

DOI:10.1159/000122056

出版商:S. Karger AG    

年代:1972

数据来源: Karger