Characterization of Rat Pituitary Cells by Their Responses to Hypothalamic Releasing Hormones

Kasahara, Kanji; Tasaka, Keiichi; Masumoto, Nobuyuki; Mizuki, Jirou; Tahara, Masahiro; Miyake, Akira; Takahashi, Osamu

doi:10.1006/bbrc.1994.1391

Cited by 20 publications

(15 citation statements)

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“…In the rat, G nR H stimulates the release of PRL and GH during a limited period in neonatal life (Andries Si Denef 1995). Moreover, a subpopulation of the gonadotrophs (identified as G nRH receptor-and gonadotrophin mRNA-positive cells) also contain the GH antigen (Childs et al 1994), and some of the gonadotrophs that 2 respond to GnRH by displaying an increase in [Ca Jj respond to GH-releasing factor (GRF) as well (Kasahara et al 1994). However, GH antigen may be bound to GH receptors on gonadotrophs and may exert a paracrine effect, as is suggested by the modulatory effect of human GH on the gonadotrophs* physiology in transgenic mice bearing the human GH gene (Chandrashekar et al 1988).…”

Section: A Pmentioning

confidence: 99%

Gonadotrophs but not somatotrophs carry gonadotrophin-releasing hormone receptors: receptor localisation, intracellular calcium, and gonadotrophin and GH release

Bosma¹,

Kolk²,

Rebers³

et al. 1997

Journal of Endocrinology

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Gonadotrophs are the primary target cells for GnRH in the pituitary. However, during a limited period of neonatal life in the rat, lactotrophs and somatotrophs respond to GnRH as well. Also, in the adults of a number of teleost fishes (e.g. carp, goldfish, and tilapia but not trout), GnRH is a potent GH secretagogue. In studying hypophysiotrophic actions of the two forms of GnRH present in the African catfish (Clarias gariepinus), chicken GnRH-II ([His5,Trp7,TyrK ] GnRH; cGnRH-II) and catfish GnRH ([His5,Asn8]GnRH; cfGnRH), we have investigated the effects of G nRH on catfish gonadotrophs and somato trophs. G nRH binding was examined by incubating dispersed pituitary cells attached to coverslips with 125I~ labelled [D-Argr\T rp 7,LeuH ,Pro9-Net]GnRH (sGnRHa), a salmon G nRH analogue with high affinity for the G nRH receptor. Following fixation and immunohistochemistry using antisera against catfish LH and GH, 125I-labelled sGnRHa was localised autoradiographically and silver grains were quantified on gonadotrophs and somatotrophs. Specific binding of ' I-labelled sGnRHa was restricted to gonadotrophs. Both cfGnRH andcGnRH~II dose-dependently inhibited I-labelled sGnRHa binding to gonadotrophs. To substantiate the localisation of functional G nR H receptors, the effects of cfGnRH and cG nR H -II on the cytosolic free calcium concentration ([Ca ' were examined in Fura-2-loaded somatotrophs and gonadotrophs. GnRH-induced increases in [Ca2+]i appeared to be confined to gonadotrophs, in which both endogenous GnRHs caused a single and transient increase in [Ca2*]}. The amplitude of this [Ca2+]j transient depended on the G nR H dose and correlated well with the G nR H s1 effect on LH release. In vivo experiments demonstrated that G nR H treatments which markedly elevated plasma LH levels had no effect on plasma GH levels, while a dopamine agonist (apomorphine) significantly elevated plasma GH levels. W e con clude that the two endogenous forms of G nR H in the African catfish are not directly involved in the regulation of the release of GH, suggesting that GnRHs cannot be considered as GH secretagogues in teleosts in general.

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Section: A Pmentioning

confidence: 99%

Gonadotrophs but not somatotrophs carry gonadotrophin-releasing hormone receptors: receptor localisation, intracellular calcium, and gonadotrophin and GH release

Bosma¹,

Kolk²,

Rebers³

et al. 1997

Journal of Endocrinology

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“…However, this traditional view of univocal regulation of pituitary hormone secretion by its specific HRH has been revisited in the last 10 years. In fact, recent studies [17,30,31] have proven that different functional cell types of the anterior pituitary can respond to a single HRH, and pituitary cells of the same functional type can respond to two or more HRHs. Thyrotropin-releasing hormone (TRH), in addition to regulating thyroid-stimulating hormone (TSH) release, is a potent releaser of prolactin (PRL) [15] and, under some circumstances, of luteinizing hormone (LH) [9] and growth hormone (GH) [12,32].…”

Section: Introductionmentioning

confidence: 99%

Detection of gonadotropin-releasing hormone receptor in normal human pituitary cells and pituitary adenomas using immunohistochemistry

Rosa¹,

Celato

Uccella

et al. 2000

Virchows Archiv

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Gonadotropin-releasing hormone (GnRH), which is a well-known regulator of gonadotroph function, has recently been considered to be a paracrine factor involved in the control of somatotroph, lactotroph, and corticotroph cells. GnRH action is initiated by binding to a specific cell surface receptor, the gonadotropin-releasing hormone receptor (GnRHR), which is expressed by follicle-stimulating hormone/luteinizing hormone (FSH/LH) cells. Using in situ hybridization techniques, GnRHR messenger ribonucleic acid (mRNA) has recently been detected in normal human anterior pituitary gland and in various pituitary adenomas, including FSH/LH-cell, growth hormone (GH)-cell, adrenocorticotropic hormone (ACTH)-cell, and null-cell adenomas. However, immunohistochemical studies indicating the specific cell distribution of GnRHR in normal pituitary cells have never been reported. The aim of the present investigation was to evaluate the immunohistochemical expression of GnRHR in different types of normal pituitary cells and related tumors. Using double-label immunohistochemical techniques on formalin-fixed and paraffin-embedded tissues and specific antibodies directed against pituitary hormones and GnRHR, we found GnRHR immunoreactivity not only in FSH/LH cells, but also in GH- and thyroid-stimulating hormone (TSH) cells. GnRHR was detected in FSH/LH-cell, GH-cell, mixed GH- and prolactin (PRL)-cell, and alpha-subunit (alpha-SU)/null-cell adenomas. The findings of this study suggest that the interaction between GnRH and GnRHR may play a role in paracrine/autocrine regulation of different types of normal pituitary cells and pituitary adenomas.

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“…More specifically, when attempts were made to characterize AP cell phenotypes on the basis of their cytosolic calcium concentration ([Ca 2ϩ ] i ) responses to HRH stimulation, many cells were found to respond to two or more of these agents (4,5). These findings not only cast doubts on the utility of [Ca 2ϩ ] i responses as an index of AP cell phenotype, but also raised a couple of interesting questions.…”

mentioning

confidence: 99%

Multi-responsiveness of single anterior pituitary cells to hypothalamic-releasing hormones: A cellular basis for paradoxical secretion

Alonso

Núñez

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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The classic view for hypothalamic regulation of anterior pituitary (AP) hormone secretion holds that release of each AP hormone is controlled specifically by a corresponding hypothalamic-releasing hormone (HRH). In this scenario, binding of a given HRH (thyrotropin-, growth hormone-, corticotropin-, and luteinizing hormone-releasing hormones) to specific receptors in its target cell increases the concentration of cytosolic Ca 2؉ ([Ca 2؉ ] i ), thereby selectively stimulating the release of the appropriate hormone. However, ''paradoxical'' responses of AP cells to the four wellestablished HRHs have been observed repeatedly with both in vivo and in vitro systems, raising the possibility of functional overlap between the different AP cell types. To explore this possibility, we evaluated the effects of HRHs on [Ca 2؉ ] i in single AP cells identified immunocytochemically by the hormone they stored. We found that each of the five major AP cell types contained discrete subpopulations that were able to respond to several HRHs. The relative abundance of these multi-responsive cells was 59% for lactotropes, 33% for thyrotropes, and in the range of 47-55% for gonadotropes, corticotropes, and somatotropes. Analysis of prolactin release from single living cells revealed that each of the four HRHs tested were able to induce hormone release from a discrete lactotrope subpopulation, the size of which corresponded closely to that in which [Ca 2؉ ] i changes were induced by the same secretagogues. When viewed as a whole, our diverse functional measurements of multi-responsiveness suggest that hypothalamic control of pituitary function is more complicated than previously envisioned. Moreover, they provide a cellular basis for the so-called ''paradoxical'' behavior of pituitary cells to hypothalamic hypophysiotropic agents.The pituitary gland is a major neuroendocrine modulator that regulates many peripheral glands and tissues through the secretion of anterior pituitary (AP) hormones. These hormones include prolactin (PRL), growth hormone (GH), thyrotropin (TSH), adrenocorticotropin, and the gonadotropins [follicle-stimulating hormone (FSH) and luteinizing hormone (LH)]. The secretory activity of the gland is controlled, in turn, by signals derived from the hypothalamus in the form of hypothalamic-releasing hormones (HRHs) such as thyrotropin-releasing hormone (TRH), growth hormone-releasing hormone (GHRH), corticotropin-releasing hormone (CRH), and gonadotropin-releasing hormone (LHRH). The classic view for hypothalamic control of AP hormone secretion holds that each major HRH modulates the secretion of a single pituitary hormone (1), but there are some notable exceptions to this rule. For example, TRH is acknowledged to be a physiological modulator of both TSH and PRL secretion, just as LHRH controls the release of both LH and FSH. In addition to these acknowledged exceptions, there have been sporadic reports about ''paradoxical'' responses to various HRHs. Such observations of AP hormone release elicited by a noncorresp...

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Characterization of Rat Pituitary Cells by Their Responses to Hypothalamic Releasing Hormones

Cited by 20 publications

References 0 publications

Gonadotrophs but not somatotrophs carry gonadotrophin-releasing hormone receptors: receptor localisation, intracellular calcium, and gonadotrophin and GH release

Gonadotrophs but not somatotrophs carry gonadotrophin-releasing hormone receptors: receptor localisation, intracellular calcium, and gonadotrophin and GH release

Detection of gonadotropin-releasing hormone receptor in normal human pituitary cells and pituitary adenomas using immunohistochemistry

Multi-responsiveness of single anterior pituitary cells to hypothalamic-releasing hormones: A cellular basis for paradoxical secretion

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