Responses of oxytocinergic and vasopressinergic cells of the supraoptic and paraventricular nuclei of the rat hypothalamus to repeated injections of thyrotrophin releasing hormone

1984 ◽  
Vol 98 (5) ◽  
pp. 1458-1461
Author(s):  
I. A. Krasnovskaya
Keyword(s):  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Paraventricular Nuclei ◽  
Vasopressinergic Cells

ABSENCE OF PYROGLUTAMYL-N3im-METHYL-HISTIDYL-PROLINEAMIDE (METHYL-THYROTROPHIN RELEASING HORMONE) IN THE RAT HYPOTHALAMUS

1978 ◽  
Vol 77 (3) ◽  
pp. 405-408 ◽  
Author(s):  
A. E. PEKARY ◽  
J. E. MORLEY ◽  
J. M. HERSHMAN
Keyword(s):  
Cation Exchange ◽  
Exchange Chromatography ◽  
Mammalian Brain ◽  
Synthetic Analogue ◽  
Cation Exchange Chromatography ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus

Pyroglutamyl-N3im-methyl-histidyl-prolineamide (methyl-thyrotrophin releasing hormone, methyl-TRH) is a potent synthetic analogue of TRH. N3im-Methyl-histidine is present in mammalian brain and it has been suggested that methyl-TRH is a physiological releasing hormone normally present in the hypothalamus. A non-gradient cation-exchange chromatography system that uses SP-Sephadex C-25 and completely resolves methyl-TRH and TRH has been developed. Because methyl-TRH cross-reacts in the immunoassay for TRH, this assay was used to measure TRH and methyl-TRH in the chromatographic fractions. By this means it has been demonstrated that the amount of methyl-TRH present in the rat is less than 0·025 ng/hypothalamus.

PEPTIDASES IN THE RAT HYPOTHALAMUS INACTIVATING THYROTROPHIN-RELEASING HORMONE (TRH)

1975 ◽  
Vol 79 (1) ◽  
pp. 209-216 ◽  
Author(s):  
E. C. Griffiths ◽  
K. C. Hooper ◽  
S. L. Jeffcoate ◽  
N. White
Keyword(s):  
Anterior Pituitary ◽  
Female Rats ◽  
Peptidase Activity ◽  
Thyrotrophin Releasing Hormone ◽  
Male And Female ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Male And Female Rats ◽  
Specific Radioimmunoassay ◽  
The Brain

ABSTRACT Peptidases capable of inactivating thyrotrophin-releasing hormone (TRH) have been demonstrated in the hypothalamus. With the development of a specific radioimmunoassay for TRH, this method was used to further study the enzymes acting on the releasing hormone. Whole hypothalamic homogenates from male and female rats inactivated TRH, with greater peptidase activity being found in the female animals. Separation of the homogenates into particulate (microsomal and mitochondrial) and supernatant (soluble/cytoplasmic) fractions showed approximately the same amounts of enzyme activity in both fractions, while dialysis of the fractions slightly reduced the TRH peptidase activity present, suggesting that a diffusible co-factor might be partially involved in the releasing hormone's degradation. These results confirm the presence of TRH-inactivating peptidases in the rat hypothalamus and suggest that the enzymes may be involved in some way in the mechanisms by which the brain controls thyrotrophin release by the anterior pituitary.

Intraventricular administration of thyrotrophin-releasing hormone (TRH) suppresses prolactin secretion and synthesis: a possible involvement of dopamine release by TRH from rat hypothalamus

1992 ◽  
Vol 133 (1) ◽  
pp. 59-66 ◽  
Author(s):  
H. Ikegami ◽  
H. Jikihara ◽  
K. Koike ◽  
K. Morishige ◽  
H. Kurachi ◽  
...  
Keyword(s):  
Dopamine Release ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Serum Prolactin ◽  
Dependent Manner ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Prolactin Gene ◽  
Gene Transcripts

ABSTRACT The administration of thyrotrophin-releasing hormone (TRH) causes a variety of dopamine-related biological events. To understand the specific role of TRH on rat hypothalamic dopamine neurones, we examined the in-vivo effects of intraventricular (i.c.v.) infusion of TRH on the release and synthesis of prolactin in the rat pituitary gland and on the changes in binding of [3H]MeTRH and dopamine turnover rates in rat hypothalamus. We have also examined the in-vitro effects of TRH on the release of [3H]dopamine from dispersed tuberoinfundibular dopamine neurones. Female rats were treated with i.c.v. infusions of 1 μmol TRH/l daily for 1, 3 and 7 days using Alzet osmotic pumps. Following 7 days of treatment the serum prolactin concentrations were significantly decreased. A reduction in hypothalamic TRH-binding sites (Bmax) was also apparent but the dissociation constant (Kd) was unaffected. Northern blot analysis of total RNA isolated from the pituitary glands of control animals using 32P-labelled prolactin cDNA as a probe indicated the presence of three species of prolactin gene transcripts of approximately 3·7, 2·0 and 1·0 kb in size, and these were decreased by TRH treatment. We examined the turnover rate of dopamine in the rat hypothalamus when TRH was administered i.c.v. for 7 days. There was a significant increase in 3,4-dihydroxyphenylacetic acid/dopamine ratio with TRH treatment. Moreover, exposure to TRH stimulated [3H]dopamine release from rat tuberoinfundibular neurones in a time- and dose-dependent manner. Dopamine receptor antagonists such as SCH23390 and (−)sulpiride, and other neuropeptides such as vasoactive intestinal peptide and oxytocin did not affect TRH-stimulated [3H]dopamine release. These data suggest that i.c.v. administration of TRH might decrease both prolactin secretion and accumulation of prolactin gene transcripts in the pituitary by stimulating dopamine release from tuberoinfundibular neurones. Journal of Endocrinology (1992) 133, 59–66

Further studies on the inactivation of thyrotrophin releasing hormone (TRH) by enzymes in the rat hypothalamus

1980 ◽  
Vol 93 (4) ◽  
pp. 385-391 ◽  
Author(s):  
E. C. Griffiths ◽  
J. A. Kelly ◽  
N. White ◽  
S. L. Jeffcoate
Keyword(s):  
Enzyme Activity ◽  
Biologically Active ◽  
Particulate Fraction ◽  
Supernatant Fraction ◽  
Hypothalamic Area ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Polypeptide Antibiotic ◽  
Bacitracin A

Abstract. Thyrotrophin-releasing hormone (TRH) is known to be inactivated by enzymes present in the rat hypothalamus. To make a further study of the enzymes' action on the tripeptide, synthetic TRH was incubated with two hypothalamic subcellular fractions. By using a direct radioimmunoassay for TRH, the tripeptide was shown to be rapidly degraded by both supernatant and particulate fractions, with higher enzyme activity in the particulate fraction. Of several biologically-active peptides tested, only luteinizing hormone-releasing hormone was found to inhibit TRH inactivation; bacitracin, a polypeptide antibiotic, was also effective in inhibiting inactivation. Enzyme activity was highest in the middle hypothalamic area and lowest in the posterior hypothalamic area. Thin layer chromatography of the products of enzyme cleavage revealed the formation of only deamidated TRH in the supernatant fraction and the constituent amino acids (pyroGlu, His, ProNH2) and histidylproline-diketopiperazine by the particulate fraction, suggesting the presence of an amidase in the supernatant and two peptidases in the particulate fractions. These properties of the enzymes inactivating TRH may indicate that the enzymes could be of importance in regulating the endocrine and other functions attributed to this hypothalamic regulatory hormone.

SERUM THYROTROPHIN AND THE RESPONSE TO THYROTROPHIN RELEASING HORMONE IN SYMPTOMLESS AUTOIMMUNE THYROIDITIS AND IN BORDERLINE AND OVERT HYPOTHYROIDISM

1974 ◽  
Vol 75 (2) ◽  
pp. 274-285 ◽  
Author(s):  
A. Gordin ◽  
P. Saarinen ◽  
R. Pelkonen ◽  
B.-A. Lamberg
Keyword(s):  
Autoimmune Thyroiditis ◽  
Elevated Serum ◽  
Mean Value ◽  
Primary Hypothyroidism ◽  
Overt Hypothyroidism ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
The Mean ◽  
The Individual ◽  
Serum Tsh

ABSTRACT Serum thyrotrophin (TSH) was determined by the double-antibody radioimmunoassay in 58 patients with primary hypothyroidism and was found to be elevated in all but 2 patients, one of whom had overt and one clinically borderline hypothyroidism. Six (29%) out of 21 subjects with symptomless autoimmune thyroiditis (SAT) had an elevated serum TSH level. There was little correlation between the severity of the disease and the serum TSH values in individual cases. However, the mean serum TSH value in overt hypothyroidism (93.4 μU/ml) was significantly higher than the mean value both in clinically borderline hypothyroidism (34.4 μU/ml) and in SAT (8.8 μU/ml). The response to the thyrotrophin-releasing hormone (TRH) was increased in all 39 patients with overt or borderline hypothyroidism and in 9 (43 %) of the 21 subjects with SAT. The individual TRH response in these two groups showed a marked overlap, but the mean response was significantly higher in overt (149.5 μU/ml) or clinically borderline hypothyroidism (99.9 μU/ml) than in SAT (35.3 μU/ml). Thus a normal basal TSH level in connection with a normal response to TRH excludes primary hypothyroidism, but nevertheless not all patients with elevated TSH values or increased responses to TRH are clinically hypothyroid.

DIE WIRKUNG VON SYNTHETISCHEM THYROTROPHIN RELEASING HORMONE AUF DIE ENTWICKLUNG EINES EXPERIMENTELLEN EXOPHTHALMUS BEIM GOLDFISCH

1971 ◽  
Vol 68 (2) ◽  
pp. 363-366 ◽  
Author(s):  
W. Wildmeister ◽  
F. A. Horster
Keyword(s):  
Carassius Auratus ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone

ABSTRACT Gold-fishes (carassius auratus) were injected with synthetic thyrotrophin releasing hormone (TRH) in concentrations of 25 μg to 1000 μg/fish. TRH did not provoke endocrine exophthalmos.

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