HYPOTHALAMIC SECRETION OF THYROTROPHIN RELEASING HORMONE IS DECREASED IN MALE JAPANESE QUAIL EXPOSED TO LONG DAILY PHOTOPERIODS

1982 ◽  
Vol 92 (2) ◽  
pp. 261-265 ◽  
Author(s):  
O. F. X. ALMEIDA

Adult male Japanese quail held under short daily photoperiods (8 h light: 16 h darkness; 8L : 16D) had significantly higher plasma concentrations of thyroid-stimulating hormone (TSH), tri-iodothyronine (T3) and thyroxine (T4) than did those kept under long days (16L : 8D). When given a single s.c. injection of 50 μg thyrotrophin releasing hormone (TRH) the birds held under both the 8L : 16D and 16L : 8D photoperiods showed rapid increases in their blood concentrations of TSH, T4 and T3, the amplitude of the TSH response of the birds exposed to 16L : 8D being particularly marked. These results suggest that, in the male quail, long daily photoperiods produce a hypothyroid state as a result of diminished TRH secretion. The synthetic and secretory capacities of the thyroid gland and pituitary thyrotrophs are apparently unimpaired by long days.

BMJ ◽  
1970 ◽  
Vol 2 (5704) ◽  
pp. 274-277 ◽  
Author(s):  
R. Hall ◽  
J. Amos ◽  
R. Garry ◽  
R. L Buxton

1996 ◽  
Vol 17 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Anna Capaldo ◽  
Vincenza Laforgia ◽  
Rosaria Sciarrillo ◽  
Antimo Cavagnuolo

AbstractInsulin was administered to Podarcis sicula in winter, when the thyroid gland is inhibited. The activity of the thyroid increased, plasma concentrations of thyroid hormones and hepatic 5'-monodeiodinase activity (MDA) increased, and thyroid stimulating hormone (TSH) concentrations fell to undetectable values. This result confirms the influence of insulin on the activity of the thyroid gland in the lizard species studied. The mechanisms are still unclear, although there is evidence which leads us to believe that insulin is directly responsible for thyroid activation.


1989 ◽  
Vol 19 (1) ◽  
pp. 69-77 ◽  
Author(s):  
R. Hunter ◽  
J. E. Christie ◽  
L. J. Whalley ◽  
J. Bennie ◽  
S. Carroll ◽  
...  

SynopsisThe endocrine responses to Luteinizing Hormone Releasing Hormone (LHRH) of eight drug-free males with mania were determined. Basal levels of Luteinizing Hormone (LH) and the plasma levels following injection of LHRH were elevated in patients compared with controls; Follicle Stimulating Hormone (FSH) and testosterone were not different. Elevated levels of LH have been described previously in recovered manic patients and have been suggested to be state-independent features of mania. In order to clarify the status of this finding, the effects of lithium administration upon hormone responses to LHRH in six male volunteers were also investigated, together with the effects upon Thyrotrophin Releasing Hormone (TRH) stimulation of Thyroid Stimulating Hormone (TSH) and prolactin release. Lithium increased the basal levels of LH and levels after injection of LHRH without effect upon FSH and testosterone. Lithium also increased basal and TRH stimulated release of TSH and basal prolactin levels. Lithium was without effect upon prolactin responses to TRH. The results are discussed in relation to current information on the mechanism of lithium's action. The implications for neuroendocrine work on recovered patients taking lithium are also explored.


BMJ ◽  
1984 ◽  
Vol 289 (6455) ◽  
pp. 1334-1336 ◽  
Author(s):  
J Seth ◽  
H A Kellett ◽  
G Caldwell ◽  
V M Sweeting ◽  
G J Beckett ◽  
...  

1980 ◽  
Vol 86 (2) ◽  
pp. 357-362 ◽  
Author(s):  
TAKAMURA MURAKI ◽  
TERUO NAKADATE ◽  
YUKIKO TOKUNAGA ◽  
RYUICHI KATO

Morphine reduced the release of thyroid-stimulating hormone (TSH) which was stimulated by exposure to cold and by thyroidectomy as well as reducing the basal level of TSH in the serum of male rats. The inhibitory effect of morphine was antagonized by naloxone which did not enhance the basal or cold-induced TSH release. Pretreatment with morphine did not reduce the release of TSH induced by exogenous thyrotrophin-releasing hormone (TRH) but enhanced it. This effect of morphine was also antagonized by naloxone. The above results suggested that the effect of morphine in reducing levels of serum TSH was not mediated by blocking the effect of TRH on the anterior pituitary gland, but that it was probably mediated by the inhibition of the release of TRH.


1992 ◽  
Vol 132 (1) ◽  
pp. 93-100 ◽  
Author(s):  
R. Peeters ◽  
N. Buys ◽  
D. Vanmontfort ◽  
J. Van Isterdael ◽  
E. Decuypere ◽  
...  

ABSTRACT The influence of TRH and TSH injections on plasma concentrations of tri-iodothyronine (T3) and thyroxine (T4) was investigated in neonatal (injection within 0·5 h after delivery) and growing lambs and in normal, pregnant and lactating adult ewes (all 2 years old and originating from Suffolk, Milksheep and Texal cross-breeds). Neonatal lambs had higher levels of T3, T4 and GH compared with all other groups, whereas prolactin and TSH were higher in lactating ewes. In all animals, injections of TRH increased plasma concentrations of prolactin and TSH after 15 min but not of GH at any time. Small increases in T3 and T4 were observed in neonatal lambs, without any effect on the T3 and T4 ratio, after prolactin administration, whereas prolactin did not influence plasma concentrations of T3 or T4 in all other experimental groups. Similar results for thyroid hormones were obtained after TRH or TSH injections. It was therefore concluded that the effects observed after TRH challenge were mediated by the release of TSH. With the possible exception of neonatal lambs, plasma concentrations of T3 after administration of TRH or TSH were always increased before those of T4; the increase in T3 occurred within 0·5–1 h compared with 2–4 h for T4 in all experimental groups. This resulted in an increased ratio of plasma T3 to T4 up to 4 h after injection. It is concluded that, in sheep, TRH and TSH preferentially release T3 from the thyroid gland probably by a stimulatory effect of TSH on the intrathyroidal conversion of T3 to T4. Journal of Endocrinology (1992) 132, 93–100


The Lancet ◽  
1972 ◽  
Vol 299 (7742) ◽  
pp. 111-113 ◽  
Author(s):  
Louis Shenkman ◽  
Araya Suphavai ◽  
Terunori Mitsuma ◽  
CharlesS Hollander

1978 ◽  
Vol 49 (5) ◽  
pp. 650-657 ◽  
Author(s):  
Alan S. Fleischer ◽  
Daniel R. Rudman ◽  
Nettleton S. Payne ◽  
George T. Tindall

✓ Prolonged coma after head trauma is associated with depletion of 3′,5′cyclic adenosine monophosphate (cAMP) in the cerebrospinal fluid (CSF). Because cAMP has previously been implicated in neuroendocrine secretion, this study examines the pituitary-hypothalamic function in 15 adult male patients (to exclude the effects of puberty and menses) with traumatic coma lasting longer than 2 weeks. Ventricular CSF cAMP was measured at 2- to 4-day intervals for 10 to 25 days. Simultaneously, plasma hormone concentrations were also determined. In all 15 cases, CSF cAMP and plasma levels of thyroid-stimulating hormone (TSH), thyroxine (T4), free T4, triiodothyronine (T3), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone became subnormal. In 11 patients whose level of consciousness fluctuated, the reduction in plasma T4 and testosterone were proportional to both severity of coma (r > 0.81, p < 0.05) and depletion of CSF cAMP (r > 0.81, p < 0.05). In four patients who remained deeply comatose for 17 to 25 days, the hypothyroidism and hypogonadism persisted. In six patients who regained consciousness, both endocrine defects improved partially or completely. Injection of 1) thyrotrophic-releasing hormone and 2) gonadotrophic-releasing hormone elicited normal or supernormal increases in plasma concentrations of 1) TSH, and 2) LH and FSH, reduced, respectively, suggesting a suprahypophyseal deficiency. These observations demonstrate that suprahypophyseal hypothyroidism and hypogonadism may occur regularly in patients with traumatic coma lasting longer than 2 weeks.


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