Changes in brain levels of gonadotropin-releasing hormone and serum levels of gonadotropin and growth hormone in goldfish during spawning

1991 ◽  
Vol 69 (1) ◽  
pp. 182-188 ◽  
Author(s):  
K. L. Yu ◽  
C. Peng ◽  
R. E. Peter
Keyword(s):  
Growth Hormone ◽  
Temporal Correlation ◽  
Serum Levels ◽  
Gonadotropin Releasing Hormone ◽  
Neuronal System ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Floating Vegetation ◽  
Serum Gh ◽  
Sexually Mature

Changes in serum levels of gonadotropin (GtH) and growth hormone (GH) and in levels of gonadotropin-releasing hormone (GnRH) in the pituitary and discrete brain areas were studied in male goldfish during spawning with spontaneously ovulating females. Spontaneous ovulation in females was induced by raising water temperature from 12 to 20 °C and providing spawning substrate of artificial floating vegetation. Spawning occurs naturally in sexually mature male goldfish in the presence of ovulating females. Serum GtH levels in spawning male goldfish exposed to ovulatory females increased markedly in synchrony with the ovulatory GtH surge in females. There was also a significant increase in serum GH levels in the spawning males. GnRH levels in the olfactory bulbs, telencephalon, hypothalamus, and pituitary of the spawning males showed marked decreases at the same time as serum levels of both GtH and GH peaked; these events in the males corresponded to the approximate time of ovulation, and similar changes in serum GtH and GH levels and brain GnRH levels, in the females. This temporal correlation between changes in GnRH levels in the brain and pituitary and increases in serum levels of GtH and GH in males as well as females supports the idea that activation of the GnRH neuronal system may be a common pathway for the stimulation of pituitary GtH and GH secretion in goldfish during spawning.

PKC and ERK are differentially involved in gonadotropin-releasing hormone-induced growth hormone gene expression in the goldfish pituitary

2005 ◽  
Vol 289 (6) ◽  
pp. R1625-R1633 ◽  
Author(s):  
Christian Klausen ◽  
Takeshi Tsuchiya ◽  
John P. Chang ◽  
Hamid R. Habibi
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Primary Cultures ◽  
Gonadotropin Releasing Hormone ◽  
Growth Hormone Gene ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Gh Gene

Gonadotropin-releasing hormone (GnRH) is produced by the hypothalamus and stimulates the synthesis and secretion of gonadotropin hormones. In addition, GnRH also stimulates the production and secretion of growth hormone (GH) in some fish species and in humans with certain clinical disorders. In the goldfish pituitary, GH secretion and gene expression are regulated by two endogenous forms of GnRH known as salmon GnRH and chicken GnRH-II. It is well established that PKC mediates GnRH-stimulated GH secretion in the goldfish pituitary. In contrast, the signal transduction of GnRH-induced GH gene expression has not been elucidated in any model system. In this study, we demonstrate, for the first time, the presence of novel and atypical PKC isoforms in the pituitary of a fish. Moreover, our results indicate that conventional PKCα is present selectively in GH-producing cells. Treatment of primary cultures of dispersed goldfish pituitary cells with PKC activators (phorbol ester or diacylglycerol analog) did not affect basal or GnRH-induced GH mRNA levels, and two different inhibitors of PKC (calphostin C and GF109203X) did not reduce the effects of GnRH on GH gene expression. Together, these results suggest that, in contrast to secretion, conventional and novel PKCs are not involved in GnRH-stimulated increases in GH mRNA levels in the goldfish pituitary. Instead, PD98059 inhibited GnRH-induced GH gene expression, suggesting that the ERK signaling pathway is involved. The results presented here provide novel insights into the functional specificity of GnRH-induced signaling and the regulation of GH gene expression.

Mechanisms for gonadotropin-releasing hormone potentiation of growth hormone rebound following norepinephrine inhibition in goldfish pituitary cells

2007 ◽  
Vol 292 (1) ◽  
pp. E203-E214 ◽  
Author(s):  
Anderson O. L. Wong ◽  
Maggie C. Y. Chuk ◽  
Hiu Chi Chan ◽  
Eric K. Y. Lee
Keyword(s):  
Growth Hormone ◽  
Adrenergic Receptors ◽  
Gonadotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Adrenergic Stimulation ◽  
Dependent Protein Kinase ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Dependent Protein ◽  
Subsequent Activation

In the goldfish, norepinephrine (NE) inhibits growth hormone (GH) secretion through activation of pituitary α2-adrenergic receptors. Interestingly, a GH rebound is observed after NE withdrawal, which can be markedly enhanced by prior exposure to gonadotropin-releasing hormone (GnRH). Here we examined the mechanisms responsible for GnRH potentiation of this “postinhibition” GH rebound. In goldfish pituitary cells, α2-adrenergic stimulation suppressed both basal and GnRH-induced GH mRNA expression, suggesting that a rise in GH synthesis induced by GnRH did not contribute to its potentiating effect. Using a column perifusion approach, GnRH given during NE treatment consistently enhanced the GH rebound following NE withdrawal. This potentiating effect was mimicked by activation of PKC and adenylate cyclase (AC) but not by induction of Ca2+ entry through voltage-sensitive Ca2+ channels (VSCC). Furthermore, GnRH-potentiated GH rebound could be alleviated by inactivation of PKC, removal of extracellular Ca2+, blockade of VSCC, and inhibition of Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII). Inactivation of AC and PKA, however, was not effective in this regard. These results, as a whole, suggest that GnRH potentiation of GH rebound following NE inhibition is mediated by PKC coupled to Ca2+ entry through VSCC and subsequent activation of CaMKII. Apparently, the Ca2+-dependent cascades are involved in GH secretion during the rebound phase but are not essential for the initiation of GnRH potentiation. Since GnRH has been previously shown to have no effects on cAMP synthesis in goldfish pituitary cells, the involvement of cAMP-dependent mechanisms in GnRH potentiation is rather unlikely.

Changes in brain mRNA levels of gonadotropin-releasing hormone, pituitary adenylate cyclase activating polypeptide, and somatostatin during ovulatory luteinizing hormone and growth hormone surges in goldfish

2008 ◽  
Vol 295 (6) ◽  
pp. R1815-R1821 ◽  
Author(s):  
Luis Fabián Canosa ◽  
Norm Stacey ◽  
Richard Ector Peter
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Adenylate Cyclase ◽  
Feedback Mechanism ◽  
Gonadotropin Releasing Hormone ◽  
Mrna Levels ◽  
Spawning Behavior ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Pituitary Adenylate Cyclase

In goldfish, circulating LH and growth hormone (GH) levels surge at the time of ovulation. In the present study, changes in gene expression of salmon gonadotropin-releasing hormone (sGnRH), chicken GnRH-II (cGnRH-II), somatostatin (SS) and pituitary adenylate cyclase activating polypeptide (PACAP) were analyzed during temperature- and spawning substrate-induced ovulation in goldfish. The results demonstrated that increases in PACAP gene expression during ovulation are best correlated with the GH secretion profile. These results suggest that PACAP, instead of GnRH, is involved in the control of GH secretion during ovulation. Increases of two of the SS transcripts during ovulation are interpreted as the activation of a negative feedback mechanism triggered by high GH levels. The results showed a differential regulation of sGnRH and cGnRH-II gene expression during ovulation, suggesting that sGnRH controls LH secretion, whereas cGnRH-II correlates best with spawning behavior. This conclusion is further supported by the finding that nonovulated fish induced to perform spawning behavior by prostaglandin F2α treatment increased cGnRH-II expression in both forebrain and midbrain, but decreased sGnRH expression in the forebrain.

Effects of cytidine 5'-diphosphocholine administration on basal and growth hormone-releasing hormone-induced growth hormone secretion in elderly subjects

1991 ◽  
Vol 124 (5) ◽  
pp. 516-520 ◽  
Author(s):  
Gian Paolo Ceda ◽  
Graziano Ceresini ◽  
Licia Denti ◽  
Dario Magnani ◽  
Lorenzo Marchini ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
The Elderly ◽  
Treated Group ◽  
Elderly Subjects ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Healthy Elderly ◽  
Serum Gh

Abstract. The basal and GH-releasing hormone-stimulated secretion of GH declines in the elderly. We tested the ability of cytidine 5'-diphosphocholine, a drug used in the treatment of stroke and Parkinson's disease, to alter GH secretion in 11 healthy elderly volunteers, aged 69-84. Each subject received an iv infusion of 2 g of cytidine 5'-diphosphocholine or normal saline. GHRH and TRH were also administered during cytidine 5'diphosphocholine infusions. The infusion of cytidine 5'-diphosphocholine induced a 4-fold (p<0.05) increase in serum GH levels over basal values. A small increase in GH was seen after GHRH administration. However, the addition of GHRH to the cytidine 5'-diphosphocholine infusion resulted in a GH response which was significantly greater than that seen after GHRH alone; the integrated concentration of GH was more than 2-fold greater in the cytidine 5'-diphosphocholine treated group (706.85± 185.1 vs 248.9±61.4 μg · l−1 · (120 min)−1; p=0.01). The PRL and TSH responses to TRH were not significantly affected by cytidine 5'-diphosphocholine infusion, indicating that dopaminergic mechanisms are not involved. These studies demonstrate that cytidine 5'-diphosphocholine can enhance basal and GHRH-stimulated GH release in the elderly, but the mechanism of action of the drug remains unclear.

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