| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
ARTICLES |
Department of Animal and Avian Sciences, University of Maryland, College Park, Maryland 20742
Address all correspondence and requests for reprints to: Dr. Tom E. Porter, Department of Animal and Avian Sciences, University of Maryland, College Park, Maryland 20742. E-mail: tp44{at}umail.umd.edu
We reported that corticosterone administration into the albumen of fertile chicken eggs on embryonic day (e) 11 induces an increase in the population of GH-secreting cells. The present study evaluated the ontogeny, dose response, localization, and persistence of the glucocorticoid-induced increase in the somatotroph population during chicken embryonic development. Corticosterone (0, 0.02, 0.2, and 2 µg in 300 µl saline) was injected into separate eggs on e9, e10, e11, and e12, and the population of GH-secreting cells was assessed 2 days later using reverse hemolytic plaque assays. Corticosterone treatment on e9 or e10 was unable to increase the population of GH-secreting cells on e11 or e12. In contrast, 0.2 and 2 µg of corticosterone on e11 increased the population of GH-secreting cells on e13 (P < 0.05, n = 3 experiments) to 8.2 ± 0.6 and 6.4 ± 0.5% of all cells, respectively, relative to controls (2.4 ± 0.2%). For e14 embryos treated on e12, only the 2 µg dose increased the proportion of GH-secreting cells (6.4 ± 0.6%) relative to controls (3.6 ± 0.4%). In a second experiment, 0, 0.02, 0.2, 2, and 20 µg of corticosterone were injected on e0, e8, e9, e10, e11, and e12, and the population of GH-secreting cells was assessed on e13 in all groups. No dose of corticosterone was effective when given on e0, e8, e9, or e10. The 0.2 µg and 2 µg doses increased the population of GH-secreting cells (7.6 ± 0.9% and 6.7 ± 0.8%, respectively) relative to controls (2.3 ± 0.4%) when injected on e11 (P < 0.05, n = 4 experiments). The 2-µg dose also increased GH cell abundance when injected on e12 (5.6 ± 0.4%), relative to controls (2.7 ± 0.5%). Treatment with 20 µg on e11 and e12 induced the greatest responses (10.3 ± 1.1% and 8.7 ± 0.9%, respectively). However, in subsequent experiments, administration of 20 µg on e11 resulted in embryonic death by e18. In a third set of experiments, two groups of eggs were injected either with 2 µg of corticosterone in saline or saline alone on e11, and the number of GH-secreting cells was estimated on e13, e16, e19, and the day of hatch (d1). The population of GH-secreting cells in corticosterone treated embryos was significantly higher than in saline treated embryos only on e13 (7.1 ± 0.8% and 2.7 ± 0.3%, respectively). No significant differences were observed on e16 (12.4 ± 1.5% and 13.6 ± 1.2%), e19 (19.0 ± 1.0% and 18.2 ± 1.7%) and d1 (23.8 ± 2.1% and 25.1 ± 1.8%) between corticosterone treated and control embryos, respectively. In a fourth set of experiments, whole mount in situ hybridization indicated that injection of corticosterone on e11 induced GH messenger RNA expression in the caudal part of the pituitary gland on e13, where somatotrophs are located normally later in development. We conclude that corticosterone administration in ovo can increase the population of GH-secreting cells in the caudal anterior pituitary only during a small window of development between e11 and e13 and that this premature increase of GH-secreting cells does not affect the percentage of GH-secreting cells later in development.
This article has been cited by other articles:
 |
|
 |
|
  L. E Ellestad, S. A Malkiewicz, H D. Guthrie, G. R Welch, and T. E Porter Expression and regulation of glucocorticoid-induced leucine zipper in the developing anterior pituitary gland J. Mol. Endocrinol., February 1, 2009; 42(2): 171 - 183. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Ton. G.G Groothuis and H. Schwabl Hormone-mediated maternal effects in birds: mechanisms matter but what do we know of them? Phil Trans R Soc B, May 12, 2008; 363(1497): 1647 - 1661. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. A. Cogburn, T. E. Porter, M. J. Duclos, J. Simon, S. C. Burgess, J. J. Zhu, H. H. Cheng, J. B. Dodgson, and J. Burnside Functional Genomics of the Chicken A Model Organism Poult. Sci., October 1, 2007; 86(10): 2059 - 2094. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. A. Jenkins, M. Muchow, M. P. Richards, J. P. McMurtry, and T. E. Porter Administration of Adrenocorticotropic Hormone during Chicken Embryonic Development Prematurely Induces Pituitary Growth Hormone Cells Endocrinology, August 1, 2007; 148(8): 3914 - 3921. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Muchow, I. Bossis, and T. E Porter Ontogeny of pituitary thyrotrophs and regulation by endogenous thyroid hormone feedback in the chick embryo J. Endocrinol., February 1, 2005; 184(2): 407 - 416. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
X. Fu, S. Nishimura, and T. E Porter Evidence that lactotrophs do not differentiate directly from somatotrophs during chick embryonic development J. Endocrinol., November 1, 2004; 183(2): 417 - 425. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Bossis, S. Nishimura, M. Muchow, and T. E. Porter Pituitary Expression of Type I and Type II Glucocorticoid Receptors during Chicken Embryonic Development and Their Involvement in Growth Hormone Cell Differentiation Endocrinology, July 1, 2004; 145(7): 3523 - 3531. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
X. Fu and T. E. Porter Glucocorticoid Induction of Lactotrophs and Prolactin Gene Expression in Chicken Embryonic Pituitary Cells: A Delayed Response Relative to Stimulated Growth Hormone Production Endocrinology, March 1, 2004; 145(3): 1322 - 1330. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
