scholarly journals Anterior Pituitary Transcriptome Suggests Differences in ACTH Release in Tame and Aggressive Foxes

2018 ◽  
Vol 8 (3) ◽  
pp. 859-873 ◽  
Author(s):  
Jessica P. Hekman ◽  
Jennifer L. Johnson ◽  
Whitney Edwards ◽  
Anastasiya V. Vladimirova ◽  
Rimma G. Gulevich ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Acth Release

Early glucocorticoid feedback in anterior pituitary corticotrophs: differential inhibition of hormone release induced by vasopressin and corticotrophin-releasing factor in vitro

1991 ◽  
Vol 129 (2) ◽  
pp. 261-268 ◽  
Author(s):  
M. J. Shipston ◽  
F. A. Antoni
Keyword(s):  
Anterior Pituitary ◽  
Actinomycin D ◽  
Feedback Inhibition ◽  
Female Rats ◽  
Hormone Release ◽  
Type Ii ◽  
Acth Secretion ◽  
Corticotrophin Releasing Factor ◽  
Acth Release

ABSTRACT Vasopressin and 41-residue corticotrophin-releasing factor (CRF-41) are physiological mediators of the hypothalamic control of pituitary ACTH secretion, whilst adrenocortical glucocorticoids are the major inhibitory factors regulating ACTH output. In the present study it was investigated in vitro whether the characteristics of early glucocorticoid inhibition of stimulated ACTH secretion would differ depending on the nature of the stimulus and the temporal relationship between secretagogue and steroid. The experiments were carried out using perifused segments of rat adenohypophysis obtained from randomly cycling female rats. Repeated pulses (5 min) of CRF-41 or vasopressin were given at 1-h intervals for up to 7 h. The net release of ACTH became stable after the second secretagogue pulse. Administration of 0·1 μmol corticosterone/l 30 min before and during a 5-min pulse of 10 nmol CRF-41/l inhibited CRF-41-stimulated ACTH release to 60% of control. Stimulated hormone release remained suppressed at 90 min after the start of the corticosterone infusion and returned to control levels by 150 min. If corticosterone treatment (35 min total exposure) was started simultaneously with the CRF-41 pulse, no inhibitory effect of the steroid was observed at any subsequent time-point examined (60,90,120 and 150 min). In contrast, vasopressin-stimulated ACTH release was inhibited by approximately 50% when corticosterone was applied before, or simultaneously with, a 5-min pulse of 10 nmol vasopressin/l. The synthetic glucocorticoid type II receptor agonist RU28362, administered 30 min before and during a 5-min pulse of 10 nmol CRF-41/l, reduced CRF-41-stimulated ACTH release to 50% of control up to 2·5 h after the start of RU28362 application (although inhibition after 35 min exposure was not statistically significant). Inhibition of ACTH release stimulated by 10 nmol vasopressin/l was observed within 35 min of steroid application and was maintained up to 2·5 h after the initial application of RU28362. The action of RU28362 on CRF-41-stimulated ACTH release was blocked by inhibitors of transcription (actinomycin D) and translation (puromycin); notably these drugs did not modify the ACTH response to CRF-41. In contrast, actinomycin D as well as puromycin reduced vasopressin-stimulated ACTH release. The data suggest that: (1) the timing of steroid application is important in determining the early glucocorticoid inhibition of CRF-41- but not vasopressin-stimulated ACTH secretion; (2) CRF-41 and vasopressin mobilize different pools of ACTH from the anterior pituitary gland; (3) type II glucocorticoid receptors and synthesis of new protein(s) are involved in the early inhibitory action of glucocorticoids; (4) depending on the timing and nature of the incident secretagogue, differential negative feedback inhibition of ACTH secretion may occur at the pituitary level in vivo. Journal of Endocrinology (1991) 129, 261–268

Regulation of ACTH secretory pathways in cultured pituitary cells

1991 ◽  
Vol 261 (5) ◽  
pp. C793-C798 ◽  
Author(s):  
J. Schwartz ◽  
S. Gibson ◽  
A. White
Keyword(s):  
Anterior Pituitary ◽  
Adrenocorticotropic Hormone ◽  
Corticotropin Releasing Factor ◽  
Pituitary Cells ◽  
Receptor Complex ◽  
Response Mechanism ◽  
Acth Secretion ◽  
Secretory Pathways ◽  
Anterior Pituitary Cells ◽  
Acth Release

Although chloroquine, an agent that disrupts regulated protein secretion, has previously been shown to decrease the adrenocorticotropic hormone (ACTH) secretory response to adenosine 3',5'-cyclic monophosphate or corticotropin-releasing factor (CRF) in AtT-20 and rat anterior pituitary cells, respectively, it has no effect on the response to vasopressin. The present study extended experiments with chloroquine to cultured sheep anterior pituitary cells, which have a greater maximum response to vasopressin. Chloroquine (200 microM) had no effect on basal ACTH secretion or on stimulation by vasopressin. In contrast to the rat, the net response to CRF was tripled by chloroquine in ovine cells. The effect of chloroquine on the response to CRF was more effective by coexposure of cells to CRF and chloroquine than by pretreatment with chloroquine. Monensin or vinblastine did not increase the ACTH response to CRF. The results indicate ACTH release in response to vasopressin is chloroquine insensitive in this way, can be dissociated from the mechanism that responds to CRF, and would be consistent with the CRF response mechanism involving pathways that can alter the secretory pool of ACTH. When chloroquine acts to increase the response to CRF, it is likely not to act by stabilizing the CRF-receptor complex.

Blockage of K+ channels reverses the inhibitory action of atriopeptin on secretagogue-stimulated ACTH release by perifused isolated rat anterior pituitary cells

1990 ◽  
Vol 126 (2) ◽  
pp. 183-191 ◽  
Author(s):  
F. A. Antoni ◽  
G. Dayanithi
Keyword(s):  
Anterior Pituitary ◽  
Inhibitory Action ◽  
Calcium Ionophore ◽  
Delayed Rectifier ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Acth Secretion ◽  
Anterior Pituitary Cells ◽  
Isolated Rat ◽  
Acth Release

ABSTRACT The aim of the present study was to investigate how atriopeptin inhibits secretagogue-stimulated ACTH secretion in vitro. Perifused isolated rat anterior pituitary cells were used throughout; the ACTH content of the perifusate was measured by radioimmunoassy. In the presence of a constant (0·05 nmol/l) concentration of 41-residue corticotrophin-releasing factor (CRF), arginine vasopressin (AVP; 0·05–50 nmol/l) stimulated ACTH secretion in a concentration-dependent manner, the combination of 0·05 nmol CRF/l and 0·5 nmol AVP/l (CRF/AVP) stimulated ACTH release to six- to eightfold above baseline. The effect of CRF/AVP was not modified by tetrodotoxin, but was abolished by CoCl2 and reduced to about 70% of the control stimulus by nifedipine. Application of 103–126 residue atriopeptin for 10 min before and 2·5 min during the CRF/AVP stimulus strongly suppressed the evoked release of ACTH, the maximal inhibition was 75–90% at 10 nmol atriopeptin/l. The calcium ionophore ionomycin (200 nmol/l) reversed the effect of atriopeptin while it had no secretagogue activity of its own, and did not enhance the response to CRF/AVP. A variety of blockers of K+ channels, 4-amino pyridine, tetraethylammonium, apamine, quinine, but not tolbutamide, effectively antagonized the inhibitory action of atriopeptin (10 nmol/l). None of these drugs altered ACTH release evoked by CRF/AVP. In concentration–response experiments, the half effective concentration of 4-aminopyridine and tetraethyl-ammonium were around 1 mmol/l and 10 nmol/l for apamine. Finally, tetraethylammonium and apamine also antagonized the inhibition of CRF/AVP-evoked ACTH release by 8-Br-cGMP. These data suggest that (1) at least two types of K+ channels, a delayed rectifier and the apamine-sensitive Ca2+-activated channel, are functionally important in pituitary corticotroph cells; (2) atriopeptin inhibits CRF/AVP-stimulated ACTH secretion by hyperpolarizing the plasma membrane and thus reducing the uptake of Ca2+ into the cells; (3) cGMP is the intracellular mediator of the action of atriopeptin on corticotroph cells. Journal of Endocrinology (1990) 126, 183–191

Effect of S(−)- and R(+)-salsolinol on the POMC gene expression and ACTH release of an anterior pituitary cell line

Alcohol ◽  
1995 ◽  
Vol 12 (5) ◽  
pp. 447-452 ◽  
Author(s):  
Ingo Putscher ◽  
Hanka Haber ◽  
Anett Winkler ◽  
Jörns Fickel ◽  
Matthias F. Melzig
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
Anterior Pituitary ◽  
Pituitary Cell ◽  
Anterior Pituitary Cell ◽  
Pomc Gene ◽  
Acth Release

scholarly journals Fear and Foxes: An Educational Primer for Use with “Anterior Pituitary Transcriptome Suggests Differences in ACTH Release in Tame and Aggressive Foxes”

Genetics ◽  
2020 ◽  
Vol 215 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Julie H. Simpson
Keyword(s):  
Anterior Pituitary ◽  
Selective Breeding ◽  
Association Studies ◽  
Model Organisms ◽  
Genome Wide Association Studies ◽  
Behavioral Differences ◽  
Genetic Changes ◽  
Genome Wide ◽  
Discovery Science ◽  
Acth Release

The way genes contribute to behavior is complicated. Although there are some single genes with large contributions, most behavioral differences are due to small effects from many interacting genes. This makes it hard to identify the genes that cause behavioral differences. Mutagenesis screens in model organisms, selective breeding experiments in animals, comparisons between related populations with different behaviors, and genome-wide association studies in humans are promising and complementary approaches to understanding the heritable aspects of complex behaviors. To connect genes to behaviors requires measuring behavioral differences, locating correlated genetic changes, determining when, where, and how these candidate genes act, and designing causative confirmatory experiments. This area of research has implications from basic discovery science to human mental health.

Cellular localization of apelin and its receptor in the anterior pituitary: evidence for a direct stimulatory action of apelin on ACTH release

2007 ◽  
Vol 292 (1) ◽  
pp. E7-E15 ◽  
Author(s):  
Annabelle Reaux-Le Goazigo ◽  
Rodrigo Alvear-Perez ◽  
Philippe Zizzari ◽  
Jacques Epelbaum ◽  
Marie-Thérèse Bluet-Pajot ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Cellular Localization ◽  
Physiological Role ◽  
Nerve Fibers ◽  
Male Rat ◽  
Stimulatory Action ◽  
Receptor Mrna ◽  
Apelin Receptor ◽  
Acth Release

Apelin is a bioactive peptide recently identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ. The presence of apelin-immunoreactive nerve fibers, together with the detection of apelin receptor mRNA in the parvocellular part of the paraventricular nucleus and the stimulatory action of apelin on corticotropin-releasing hormone release, indicate that apelin modulates adrenocorticotropin (ACTH) release via an indirect action on the hypothalamus. However, a direct action of apelin in the anterior pituitary cannot be excluded. Here, we provided evidence for the existence of an apelinergic system within the adult male rat pituitary gland. Double immunofluorescence staining indicated that apelin is highly coexpressed in the anterior pituitary, mainly in corticotrophs (96.5 ± 0.3%) and to a much lower extent in somatotropes (3.2 ± 0.2%). Using in situ hybridization combined with immunohistochemistry, a high expression of apelin receptor mRNA was also found in corticotrophs, suggesting a local interaction between apelin and ACTH. In an ex vivo perifusion system of anterior pituitaries, apelin 17 (K17F, 10−6 M) significantly increased basal ACTH release by 41%, whereas apelin 10 (R10F, 10−6 M), an inactive apelin fragment, was ineffective. In addition, K17F but not R10F induced a dose-dependent increase in K+-evoked ACTH release, with maximal increase being observed for a 10−6 M concentration. Taken together, these data outline the potential role of apelin as an autocrine/paracrine-acting peptide on ACTH release and provide morphological and neuroendocrine basis for further studies that explore the physiological role of apelin in the regulation of anterior pituitary functions.

THE RELEASE OF CORTICOTROPHIN BY ANTERIOR PITUITARY TISSUE IN VITRO

1955 ◽  
Vol 33 (1) ◽  
pp. 408-415 ◽  
Author(s):  
Murray Saffran ◽  
A. V. Schally
Keyword(s):  
Anterior Pituitary ◽  
Brain Cortex ◽  
Test System ◽  
Posterior Pituitary ◽  
Acetyl Choline ◽  
Pituitary Tissue ◽  
Hypothalamic Tissue ◽  
Stimulation Of ◽  
Acth Release

The release of ACTH by rat anterior pituitary tissue in vitro was used as a test system for the detection of factors that stimulate ACTH-release. The results indicate that:1. Epinephrine or arterenol, added by themselves, are without effect.2. Hypothalamic tissue alone is also ineffective.3. The combination of hypothalamic tissue with epinephrine or arterenol increases the release of ACTH about threefold.4. Brain cortex can replace hypothalamus.5. Liver cannot replace neural tissue; acetyl choline and serotonin cannot replace epinephrine or arterenol.6. The greatest stimulation of ACTH-release (six- to eight-fold) occurs with posterior pituitary tissue plus arterenol. The arterenol may be replaced by hypothalamus or sphingosine, but not by dopamine (3,4-dihydroxyphenylethylamine), which is structurally similar to arterenol.7. The posterior pituitary is probably involved in the response of the anterior pituitary–adrenocortical system to stress.

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