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Sakae Kikuyama - One of the best experts on this subject based on the ideXlab platform.
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bisphenol a acts differently from and independently of thyroid hormone in suppressing Thyrotropin Release from the bullfrog pituitary
General and Comparative Endocrinology, 2008Co-Authors: Miyoko Kaneko, Reiko Okada, Kazutoshi Yamamoto, Masahisa Nakamura, Gilberto Mosconi, Alberta Maria Polzonettimagni, Sakae KikuyamaAbstract:Abstract The objective of this investigation was to ascertain whether bisphenol A (BPA), which has a structural resemblance to thyroid hormone (TH), acts as a TH agonist or antagonist in terms of affecting the Release of Thyrotropin (TSH). To this end, we exposed adult bullfrog ( Rana catesbeiana ) pituitary cells to BPA and/or TH in the presence or absence of corticotropin-releasing factor (CRF), which is known to have a potent TSH-releasing activity in amphibians. BPA (10 −9 –10 −4 M) did not affect the basal Release of TSH. However, it suppressed CRF-inducible TSH Release at 10 −4 M, but not at 10 −5 M. Triiodothyronine (T 3 ) at 10 −7 M and l -thyroxine (T 4 ) at 10 −6 M also suppressed the CRF-inducible Release of TSH. The combination of T 3 (10 −7 M) or T 4 (10 −6 M) with BPA (10 −4 M) had an additive effect in suppressing TSH Release. A comparison of the suppressive effects of BPA and T 3 on the Release of TSH following the addition of actinomycin D or cycloheximide to the culture medium revealed that both of the latter compounds blocked T 3 -inducible but not BPA-inducible suppression of TSH Release. The results indicate that the mechanism of action of BPA is different from that of T 3 in that T 3 action involves RNA and protein synthesis, whereas BPA action does not involve either of these processes. Furthermore, BPA was found to suppress the Thyrotropin-releasing hormone-inducible Release of both prolactin (PRL) and TSH. Our results suggest that BPA acts not only as a blocker of TSH secretagogues but also as a blocker of a PRL secretagogue at the pituitary level. Estradiol affected neither the Release of TSH nor the Release of PRL in the presence or absence of their secretagogues, suggesting that the suppression of the Release of TSH and PRL caused by BPA may not be derived from its estrogenic activity.
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Involvement of the corticotropin-releasing factor (CRF) type 2 receptor in CRF-induced Thyrotropin Release by the amphibian pituitary gland
General and Comparative Endocrinology, 2006Co-Authors: Reiko Okada, Mark F. Miller, Bert De Groef, Kazutoshi Yamamoto, Robert J. Denver, Sakae KikuyamaAbstract:Abstract Corticotropin-releasing factor (CRF) is considered to be a main adrenocorticotropin-releasing factor in vertebrates. In non-mammalian species, CRF and related peptides cause the Release of thyroid-stimulating hormone (TSH) from the anterior pituitary. The actions of CRF peptides are mediated by two G protein coupled receptors (CRF1 and CRF2) that have different ligand specificities. Using ligands that bind preferentially or selectively to the CRF2 we tested the hypothesis that TSH Release by the amphibian pituitary gland is mediated by the CRF2. Injection of frog CRF, urocortin 1 or the CRF2-specific ligand urocortin 3 all produced significant, acute increases (by 2 h) in plasma thyroxine concentration in prometamorphic tadpoles. Chronic injections of CRF peptides accelerated tadpole metamorphosis, and the peptides with the highest affinity for the CRF2 (urocortin 1 and sauvagine) had the greatest potency. Ligands selective for the CRF2 (frog urocortin 3, mouse urocortins 2 and 3) all accelerated tadpole metamorphosis. We then tested frog urocortins 1 and 3, mouse urocortin 2 and sauvagine for their TSH-releasing activity using dispersed frog anterior pituitary cells in culture. All of the peptides tested markedly enhanced the Release of TSH. Secretagogue-induced TSH Release was completely blocked by the general CRF receptor antagonist astressin or the CRF2-specific antagonist antisauvagine-30. Conversely, the type 1 CRF receptor-specific antagonist antalarmin had no effect on TSH secretion. Our results support the hypothesis that CRF-induced TSH Release by the amphibian pituitary gland is mediated by the CRF2.
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thyroid hormones inhibit frog corticotropin releasing factor induced Thyrotropin Release from the bullfrog pituitary in vitro
General and Comparative Endocrinology, 2005Co-Authors: Miyoko Kaneko, Reiko Okada, Kazutoshi Yamamoto, Hitomi Fujisawa, Masahisa Nakamura, Sakae KikuyamaAbstract:Abstract Due to the lack of a radioimmunoassay (RIA) system for amphibian Thyrotropin (TSH), no direct evidence that thyroid hormone suppresses the Release of TSH from the amphibian pituitary has been obtained. However, we recently developed an RIA for bullfrog ( Rana catesbeiana ) TSH and thus were able to study the effect of thyroid hormone on the Release of TSH from the bullfrog pituitary. Enzymatically dispersed pituitary cells of larval, juvenile, and adult bullfrogs were cultured in the absence or presence of 100 nM corticotropin-releasing factor of bullfrog origin (fCRF), which is known to be a potent stimulator of the Release of TSH. The amount of spontaneously Released TSH was higher in late prometamorphic and climactic tadpoles than in early prometamorphic larvae and juvenile and adult frogs. Pituitary cells from tadpoles at metamorphic climax responded to fCRF to Release much more TSH than those from early and late prometamorphic tadpoles and juvenile and adult frogs. In all cases, the fCRF (100 nM)-induced, but not the basal, Release of TSH was significantly suppressed by 1 nM triiodothyronine (T 3 ) and 1000 nM thyroxine (T 4 ), when examined using adult pituitary cells. The suppressive effect of thyroid hormones was revealed to be dependent on their concentrations.
Reiko Okada - One of the best experts on this subject based on the ideXlab platform.
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bisphenol a acts differently from and independently of thyroid hormone in suppressing Thyrotropin Release from the bullfrog pituitary
General and Comparative Endocrinology, 2008Co-Authors: Miyoko Kaneko, Reiko Okada, Kazutoshi Yamamoto, Masahisa Nakamura, Gilberto Mosconi, Alberta Maria Polzonettimagni, Sakae KikuyamaAbstract:Abstract The objective of this investigation was to ascertain whether bisphenol A (BPA), which has a structural resemblance to thyroid hormone (TH), acts as a TH agonist or antagonist in terms of affecting the Release of Thyrotropin (TSH). To this end, we exposed adult bullfrog ( Rana catesbeiana ) pituitary cells to BPA and/or TH in the presence or absence of corticotropin-releasing factor (CRF), which is known to have a potent TSH-releasing activity in amphibians. BPA (10 −9 –10 −4 M) did not affect the basal Release of TSH. However, it suppressed CRF-inducible TSH Release at 10 −4 M, but not at 10 −5 M. Triiodothyronine (T 3 ) at 10 −7 M and l -thyroxine (T 4 ) at 10 −6 M also suppressed the CRF-inducible Release of TSH. The combination of T 3 (10 −7 M) or T 4 (10 −6 M) with BPA (10 −4 M) had an additive effect in suppressing TSH Release. A comparison of the suppressive effects of BPA and T 3 on the Release of TSH following the addition of actinomycin D or cycloheximide to the culture medium revealed that both of the latter compounds blocked T 3 -inducible but not BPA-inducible suppression of TSH Release. The results indicate that the mechanism of action of BPA is different from that of T 3 in that T 3 action involves RNA and protein synthesis, whereas BPA action does not involve either of these processes. Furthermore, BPA was found to suppress the Thyrotropin-releasing hormone-inducible Release of both prolactin (PRL) and TSH. Our results suggest that BPA acts not only as a blocker of TSH secretagogues but also as a blocker of a PRL secretagogue at the pituitary level. Estradiol affected neither the Release of TSH nor the Release of PRL in the presence or absence of their secretagogues, suggesting that the suppression of the Release of TSH and PRL caused by BPA may not be derived from its estrogenic activity.
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Involvement of the corticotropin-releasing factor (CRF) type 2 receptor in CRF-induced Thyrotropin Release by the amphibian pituitary gland
General and Comparative Endocrinology, 2006Co-Authors: Reiko Okada, Mark F. Miller, Bert De Groef, Kazutoshi Yamamoto, Robert J. Denver, Sakae KikuyamaAbstract:Abstract Corticotropin-releasing factor (CRF) is considered to be a main adrenocorticotropin-releasing factor in vertebrates. In non-mammalian species, CRF and related peptides cause the Release of thyroid-stimulating hormone (TSH) from the anterior pituitary. The actions of CRF peptides are mediated by two G protein coupled receptors (CRF1 and CRF2) that have different ligand specificities. Using ligands that bind preferentially or selectively to the CRF2 we tested the hypothesis that TSH Release by the amphibian pituitary gland is mediated by the CRF2. Injection of frog CRF, urocortin 1 or the CRF2-specific ligand urocortin 3 all produced significant, acute increases (by 2 h) in plasma thyroxine concentration in prometamorphic tadpoles. Chronic injections of CRF peptides accelerated tadpole metamorphosis, and the peptides with the highest affinity for the CRF2 (urocortin 1 and sauvagine) had the greatest potency. Ligands selective for the CRF2 (frog urocortin 3, mouse urocortins 2 and 3) all accelerated tadpole metamorphosis. We then tested frog urocortins 1 and 3, mouse urocortin 2 and sauvagine for their TSH-releasing activity using dispersed frog anterior pituitary cells in culture. All of the peptides tested markedly enhanced the Release of TSH. Secretagogue-induced TSH Release was completely blocked by the general CRF receptor antagonist astressin or the CRF2-specific antagonist antisauvagine-30. Conversely, the type 1 CRF receptor-specific antagonist antalarmin had no effect on TSH secretion. Our results support the hypothesis that CRF-induced TSH Release by the amphibian pituitary gland is mediated by the CRF2.
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thyroid hormones inhibit frog corticotropin releasing factor induced Thyrotropin Release from the bullfrog pituitary in vitro
General and Comparative Endocrinology, 2005Co-Authors: Miyoko Kaneko, Reiko Okada, Kazutoshi Yamamoto, Hitomi Fujisawa, Masahisa Nakamura, Sakae KikuyamaAbstract:Abstract Due to the lack of a radioimmunoassay (RIA) system for amphibian Thyrotropin (TSH), no direct evidence that thyroid hormone suppresses the Release of TSH from the amphibian pituitary has been obtained. However, we recently developed an RIA for bullfrog ( Rana catesbeiana ) TSH and thus were able to study the effect of thyroid hormone on the Release of TSH from the bullfrog pituitary. Enzymatically dispersed pituitary cells of larval, juvenile, and adult bullfrogs were cultured in the absence or presence of 100 nM corticotropin-releasing factor of bullfrog origin (fCRF), which is known to be a potent stimulator of the Release of TSH. The amount of spontaneously Released TSH was higher in late prometamorphic and climactic tadpoles than in early prometamorphic larvae and juvenile and adult frogs. Pituitary cells from tadpoles at metamorphic climax responded to fCRF to Release much more TSH than those from early and late prometamorphic tadpoles and juvenile and adult frogs. In all cases, the fCRF (100 nM)-induced, but not the basal, Release of TSH was significantly suppressed by 1 nM triiodothyronine (T 3 ) and 1000 nM thyroxine (T 4 ), when examined using adult pituitary cells. The suppressive effect of thyroid hormones was revealed to be dependent on their concentrations.
Bert De Groef - One of the best experts on this subject based on the ideXlab platform.
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Involvement of the corticotropin-releasing factor (CRF) type 2 receptor in CRF-induced Thyrotropin Release by the amphibian pituitary gland
General and Comparative Endocrinology, 2006Co-Authors: Reiko Okada, Mark F. Miller, Bert De Groef, Kazutoshi Yamamoto, Robert J. Denver, Sakae KikuyamaAbstract:Abstract Corticotropin-releasing factor (CRF) is considered to be a main adrenocorticotropin-releasing factor in vertebrates. In non-mammalian species, CRF and related peptides cause the Release of thyroid-stimulating hormone (TSH) from the anterior pituitary. The actions of CRF peptides are mediated by two G protein coupled receptors (CRF1 and CRF2) that have different ligand specificities. Using ligands that bind preferentially or selectively to the CRF2 we tested the hypothesis that TSH Release by the amphibian pituitary gland is mediated by the CRF2. Injection of frog CRF, urocortin 1 or the CRF2-specific ligand urocortin 3 all produced significant, acute increases (by 2 h) in plasma thyroxine concentration in prometamorphic tadpoles. Chronic injections of CRF peptides accelerated tadpole metamorphosis, and the peptides with the highest affinity for the CRF2 (urocortin 1 and sauvagine) had the greatest potency. Ligands selective for the CRF2 (frog urocortin 3, mouse urocortins 2 and 3) all accelerated tadpole metamorphosis. We then tested frog urocortins 1 and 3, mouse urocortin 2 and sauvagine for their TSH-releasing activity using dispersed frog anterior pituitary cells in culture. All of the peptides tested markedly enhanced the Release of TSH. Secretagogue-induced TSH Release was completely blocked by the general CRF receptor antagonist astressin or the CRF2-specific antagonist antisauvagine-30. Conversely, the type 1 CRF receptor-specific antagonist antalarmin had no effect on TSH secretion. Our results support the hypothesis that CRF-induced TSH Release by the amphibian pituitary gland is mediated by the CRF2.
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corticotropin releasing hormone crh induced Thyrotropin Release is directly mediated through crh receptor type 2 on thyrotropes
Endocrinology, 2003Co-Authors: Bert De Groef, Eduard Kuhn, Nesya Goris, Lutgarde Arckens, Veerle DarrasAbstract:CRH is known as the main stimulator of ACTH Release. In representatives of all nonmammalian vertebrates, CRH has also been shown to induce TSH secretion, acting directly at the level of the pituitary. We have investigated which cell types and receptors are involved in CRH-induced TSH Release in the chicken (Gallus gallus). Because a lack of CRH type 1 receptors (CRH-R1) on the chicken thyrotropes has been previously reported, two hypotheses were tested using in situ hybridization and perifusion studies: 1) TSH secretion might be induced in a paracrine way involving melanocortins from the corticotropes; and 2) thyrotropes might express another type of CRH-R. For the latter, we have cloned a partial cDNA encoding the chicken CRH-R2. Neither alpha-melanotropin (alpha-MSH) nor its powerful analog Nle4,d-Phe7-MSH could mimic the in vitro TSH-releasing effect of ovine CRH. The nonselective melanocortin receptor blocker SHU91199 did not influence CRH- or TRH-induced TSH secretion. On the other hand, we have found that thyrotropes express CRH-R2 mRNA. The involvement of this CRH receptor in the response of thyrotropes to CRH was further confirmed by the fact that TSH Release was stimulated by human urocortin III, a CRH-R2-specific agonist, whereas the TSH response to CRH was completely blocked by the CRH-R blocker astressin and the CRH-R2-specific antagonist antisauvagine-30. We conclude that CRH-induced TSH secretion is mediated by CRH-R2 expressed on thyrotropes.
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in vitro study of corticotropin releasing hormone induced Thyrotropin Release ontogeny and inhibition by somatostatin
General and Comparative Endocrinology, 2003Co-Authors: Kris L Geris, Bert De Groef, Eduard Kuhn, Veerle DarrasAbstract:Recent research has shown that in the chicken important interactions take place between the adrenal and the thyroidal axis both at the central and the peripheral level. In vivo as well as in vitro experiments showed that ovine corticotropin-releasing hormone (oCRH) clearly increases Thyrotropin (TSH) secretion in late embryonic and early posthatch chicks. In vivo experiments in older chickens, however, suggested that this response might disappear at a later stage. Therefore we started to study in detail the ontogeny of the TSH releasing activity of oCRH using the in vitro perifusion technique. Several embryonic stages (E14, E16, and E18) as well as posthatch stages (C1, C8, C22, and adult chickens) were included in the study. We also investigated the possible regulatory role of somatostatin (SRIH) in this specific endocrine function of CRH. The perifusion studies show that CRH stimulated the TSH Release at all stages tested. The 10 and 100 nM oCRH doses were almost equally effective at the early embryonic stages while in most posthatch stages the higher oCRH dose was significantly more effective than the lower one. The stimulation factor, representative for the relative increase in TSH secretion following oCRH challenge, was high at early embryonic stages and clearly lower in adult animals. This seemed to be related to an age-dependent increase in basal TSH secretion levels. In both embryonic (E19) and posthatch (C8) chicks a pretreatment of the pituitaries with SRIH lowered the sensitivity of the thyrotropes to an oCRH challenge. This effect was more pronounced in the posthatch chicks compared to the embryos. The results show that CRH is capable of stimulating the TSH secretion during the entire life cycle of the chicken and that SRIH may play an important role in the fine-tuning of this response by lowering the sensitivity of the thyrotropes to CRH.
Kazutoshi Yamamoto - One of the best experts on this subject based on the ideXlab platform.
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bisphenol a acts differently from and independently of thyroid hormone in suppressing Thyrotropin Release from the bullfrog pituitary
General and Comparative Endocrinology, 2008Co-Authors: Miyoko Kaneko, Reiko Okada, Kazutoshi Yamamoto, Masahisa Nakamura, Gilberto Mosconi, Alberta Maria Polzonettimagni, Sakae KikuyamaAbstract:Abstract The objective of this investigation was to ascertain whether bisphenol A (BPA), which has a structural resemblance to thyroid hormone (TH), acts as a TH agonist or antagonist in terms of affecting the Release of Thyrotropin (TSH). To this end, we exposed adult bullfrog ( Rana catesbeiana ) pituitary cells to BPA and/or TH in the presence or absence of corticotropin-releasing factor (CRF), which is known to have a potent TSH-releasing activity in amphibians. BPA (10 −9 –10 −4 M) did not affect the basal Release of TSH. However, it suppressed CRF-inducible TSH Release at 10 −4 M, but not at 10 −5 M. Triiodothyronine (T 3 ) at 10 −7 M and l -thyroxine (T 4 ) at 10 −6 M also suppressed the CRF-inducible Release of TSH. The combination of T 3 (10 −7 M) or T 4 (10 −6 M) with BPA (10 −4 M) had an additive effect in suppressing TSH Release. A comparison of the suppressive effects of BPA and T 3 on the Release of TSH following the addition of actinomycin D or cycloheximide to the culture medium revealed that both of the latter compounds blocked T 3 -inducible but not BPA-inducible suppression of TSH Release. The results indicate that the mechanism of action of BPA is different from that of T 3 in that T 3 action involves RNA and protein synthesis, whereas BPA action does not involve either of these processes. Furthermore, BPA was found to suppress the Thyrotropin-releasing hormone-inducible Release of both prolactin (PRL) and TSH. Our results suggest that BPA acts not only as a blocker of TSH secretagogues but also as a blocker of a PRL secretagogue at the pituitary level. Estradiol affected neither the Release of TSH nor the Release of PRL in the presence or absence of their secretagogues, suggesting that the suppression of the Release of TSH and PRL caused by BPA may not be derived from its estrogenic activity.
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Involvement of the corticotropin-releasing factor (CRF) type 2 receptor in CRF-induced Thyrotropin Release by the amphibian pituitary gland
General and Comparative Endocrinology, 2006Co-Authors: Reiko Okada, Mark F. Miller, Bert De Groef, Kazutoshi Yamamoto, Robert J. Denver, Sakae KikuyamaAbstract:Abstract Corticotropin-releasing factor (CRF) is considered to be a main adrenocorticotropin-releasing factor in vertebrates. In non-mammalian species, CRF and related peptides cause the Release of thyroid-stimulating hormone (TSH) from the anterior pituitary. The actions of CRF peptides are mediated by two G protein coupled receptors (CRF1 and CRF2) that have different ligand specificities. Using ligands that bind preferentially or selectively to the CRF2 we tested the hypothesis that TSH Release by the amphibian pituitary gland is mediated by the CRF2. Injection of frog CRF, urocortin 1 or the CRF2-specific ligand urocortin 3 all produced significant, acute increases (by 2 h) in plasma thyroxine concentration in prometamorphic tadpoles. Chronic injections of CRF peptides accelerated tadpole metamorphosis, and the peptides with the highest affinity for the CRF2 (urocortin 1 and sauvagine) had the greatest potency. Ligands selective for the CRF2 (frog urocortin 3, mouse urocortins 2 and 3) all accelerated tadpole metamorphosis. We then tested frog urocortins 1 and 3, mouse urocortin 2 and sauvagine for their TSH-releasing activity using dispersed frog anterior pituitary cells in culture. All of the peptides tested markedly enhanced the Release of TSH. Secretagogue-induced TSH Release was completely blocked by the general CRF receptor antagonist astressin or the CRF2-specific antagonist antisauvagine-30. Conversely, the type 1 CRF receptor-specific antagonist antalarmin had no effect on TSH secretion. Our results support the hypothesis that CRF-induced TSH Release by the amphibian pituitary gland is mediated by the CRF2.
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thyroid hormones inhibit frog corticotropin releasing factor induced Thyrotropin Release from the bullfrog pituitary in vitro
General and Comparative Endocrinology, 2005Co-Authors: Miyoko Kaneko, Reiko Okada, Kazutoshi Yamamoto, Hitomi Fujisawa, Masahisa Nakamura, Sakae KikuyamaAbstract:Abstract Due to the lack of a radioimmunoassay (RIA) system for amphibian Thyrotropin (TSH), no direct evidence that thyroid hormone suppresses the Release of TSH from the amphibian pituitary has been obtained. However, we recently developed an RIA for bullfrog ( Rana catesbeiana ) TSH and thus were able to study the effect of thyroid hormone on the Release of TSH from the bullfrog pituitary. Enzymatically dispersed pituitary cells of larval, juvenile, and adult bullfrogs were cultured in the absence or presence of 100 nM corticotropin-releasing factor of bullfrog origin (fCRF), which is known to be a potent stimulator of the Release of TSH. The amount of spontaneously Released TSH was higher in late prometamorphic and climactic tadpoles than in early prometamorphic larvae and juvenile and adult frogs. Pituitary cells from tadpoles at metamorphic climax responded to fCRF to Release much more TSH than those from early and late prometamorphic tadpoles and juvenile and adult frogs. In all cases, the fCRF (100 nM)-induced, but not the basal, Release of TSH was significantly suppressed by 1 nM triiodothyronine (T 3 ) and 1000 nM thyroxine (T 4 ), when examined using adult pituitary cells. The suppressive effect of thyroid hormones was revealed to be dependent on their concentrations.
Veerle Darras - One of the best experts on this subject based on the ideXlab platform.
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corticotropin releasing hormone crh induced Thyrotropin Release is directly mediated through crh receptor type 2 on thyrotropes
Endocrinology, 2003Co-Authors: Bert De Groef, Eduard Kuhn, Nesya Goris, Lutgarde Arckens, Veerle DarrasAbstract:CRH is known as the main stimulator of ACTH Release. In representatives of all nonmammalian vertebrates, CRH has also been shown to induce TSH secretion, acting directly at the level of the pituitary. We have investigated which cell types and receptors are involved in CRH-induced TSH Release in the chicken (Gallus gallus). Because a lack of CRH type 1 receptors (CRH-R1) on the chicken thyrotropes has been previously reported, two hypotheses were tested using in situ hybridization and perifusion studies: 1) TSH secretion might be induced in a paracrine way involving melanocortins from the corticotropes; and 2) thyrotropes might express another type of CRH-R. For the latter, we have cloned a partial cDNA encoding the chicken CRH-R2. Neither alpha-melanotropin (alpha-MSH) nor its powerful analog Nle4,d-Phe7-MSH could mimic the in vitro TSH-releasing effect of ovine CRH. The nonselective melanocortin receptor blocker SHU91199 did not influence CRH- or TRH-induced TSH secretion. On the other hand, we have found that thyrotropes express CRH-R2 mRNA. The involvement of this CRH receptor in the response of thyrotropes to CRH was further confirmed by the fact that TSH Release was stimulated by human urocortin III, a CRH-R2-specific agonist, whereas the TSH response to CRH was completely blocked by the CRH-R blocker astressin and the CRH-R2-specific antagonist antisauvagine-30. We conclude that CRH-induced TSH secretion is mediated by CRH-R2 expressed on thyrotropes.
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in vitro study of corticotropin releasing hormone induced Thyrotropin Release ontogeny and inhibition by somatostatin
General and Comparative Endocrinology, 2003Co-Authors: Kris L Geris, Bert De Groef, Eduard Kuhn, Veerle DarrasAbstract:Recent research has shown that in the chicken important interactions take place between the adrenal and the thyroidal axis both at the central and the peripheral level. In vivo as well as in vitro experiments showed that ovine corticotropin-releasing hormone (oCRH) clearly increases Thyrotropin (TSH) secretion in late embryonic and early posthatch chicks. In vivo experiments in older chickens, however, suggested that this response might disappear at a later stage. Therefore we started to study in detail the ontogeny of the TSH releasing activity of oCRH using the in vitro perifusion technique. Several embryonic stages (E14, E16, and E18) as well as posthatch stages (C1, C8, C22, and adult chickens) were included in the study. We also investigated the possible regulatory role of somatostatin (SRIH) in this specific endocrine function of CRH. The perifusion studies show that CRH stimulated the TSH Release at all stages tested. The 10 and 100 nM oCRH doses were almost equally effective at the early embryonic stages while in most posthatch stages the higher oCRH dose was significantly more effective than the lower one. The stimulation factor, representative for the relative increase in TSH secretion following oCRH challenge, was high at early embryonic stages and clearly lower in adult animals. This seemed to be related to an age-dependent increase in basal TSH secretion levels. In both embryonic (E19) and posthatch (C8) chicks a pretreatment of the pituitaries with SRIH lowered the sensitivity of the thyrotropes to an oCRH challenge. This effect was more pronounced in the posthatch chicks compared to the embryos. The results show that CRH is capable of stimulating the TSH secretion during the entire life cycle of the chicken and that SRIH may play an important role in the fine-tuning of this response by lowering the sensitivity of the thyrotropes to CRH.
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adrenal inhibition of corticotropin releasing hormone induced Thyrotropin Release a comparative study in pre and posthatch chicks
Journal of Experimental Zoology, 1999Co-Authors: Kris L Geris, Eduard Kuhn, A Laheye, Luc Berghman, Veerle DarrasAbstract:Recent evidence indicates that corticotropin-releasing hormone (CRH) acts as a potent stimulator of Thyrotropin (TSH) Release in the chicken. In this study adrenal and thyroidal feedback mechanisms were studied. Administration of corticosterone 30 min prior to an ovine CRH (oCRH) challenge diminished the in vivo sensitivity of thyrotrophs to oCRH in 19-day-old chicken embryos (E19) (20 micrograms corticosterone; 2 micrograms oCRH) but not in 8-day-old chickens (C8) (40 micrograms corticosterone; 4 micrograms oCRH). At both ages studied, corticosterone (0.01 and 1 microM) did not alter the in vitro TSH response to oCRH (100 nM) indicating that an indirect mechanism is involved at the embryonic stage which is no longer present in posthatch chickens. In vitro, 3,5,3'-triiodothyronine (T3) pretreatment (0.01 and 1 microM) resulted at both ages studied in a dose-dependent drop in the in vitro oCRH-induced TSH Release. As recorded previously, corticosterone treatment provoked a rise in plasma T3 in embryonic but not in posthatch chickens. The presence of an indirect adrenal feedback mechanism in chicken embryos may therefore be linked to the increase in plasma T3 which will alter the sensitivity of thyrotrophs to hypothalamic releasing factors. In conclusion, corticosterone does not directly modulate the responsiveness of thyrotrophs to CRH, but its feedback mechanism may be dependent on the evoked increase in plasma T3 which is only present in embryonic chickens. Corticosterone may in this regard play an essential role during embryonic development by coordinating thyroidal feedback mechanisms at the level of the chicken pituitary.