| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Department of Obstetrics Gynecology and Reproductive Sciences (H.Y., P.B., R.I.W.), University of California San Francisco, San Francisco, California 94143; Department of Neurology (L.B.-P., A.C.C.), University of California Los Angeles, Los Angeles, California 90095; and Department of Obstetrics and Gynecology (M.C.), Stanford University, Stanford, California 94350
Address all correspondence and requests for reprints to: Richard Weiner, Ph.D., Department of Obstetrics, Gynecology and Reproductive Sciences, 513 Parnassus Avenue, HSE 1605, Box 0556, University of California San Francisco, San Francisco, California 94143. E-mail: weinerr{at}obgyn.ucsf.edu.
Pulsatile GnRH secretion is an intrinsic property of GnRH neurons. Since increases in cAMP levels increase excitability and GnRH secretion in the GT1–1 GnRH cell line, we asked whether cAMP levels play a role in timing excitability and intrinsic pulsatile GnRH secretion. The expression of the cAMP-specific phosphodiesterase (PDE4D1) was used in a genetic approach to lower cAMP levels. Cells were infected with an adenovirus vector (Ad) expressing PDE4D1 (PDE-Ad), or for controls with an empty Ad (Null-Ad) or an Ad expressing green fluorescent protein (GFP-Ad). Infection with the PDE-Ad significantly inhibited forskolin-induced increases in cAMP production, GnRH secretion, and Ca2+ oscillations. Infection of GT1–1 cells with the PDE-Ad vs. GFP-Ad or Null-Ad controls significantly decreased spontaneous Ca2+ oscillations and inhibited the frequency of GnRH pulses. These data support the hypothesis that the level of cAMP in GT1 neurons is a component of the biological clock timing neuron excitability and pulsatile GnRH secretion. Genetically targeted expression of PDE4D1 represents a powerful approach to study the role of cAMP levels in specific populations of neurons in transgenic animals.
This article has been cited by other articles:
 |
|
 |
|
  K. Janssens, M. Boussemaere, S. Wagner, K. Kopka, and C. Denef {beta}1-Adrenoceptors in Rat Anterior Pituitary May Be Constitutively Active. Inverse Agonism of CGP 20712A on Basal 3',5'-Cyclic Adenosine 5'-Monophosphate Levels Endocrinology, May 1, 2008; 149(5): 2391 - 2402. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Constantin and S. Wray Gonadotropin-Releasing Hormone-1 Neuronal Activity Is Independent of Cyclic Nucleotide-Gated Channels Endocrinology, January 1, 2008; 149(1): 279 - 290. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. E. Blackman, H. Yoshida, S. Paruthiyil, and R. I. Weiner Frequency of Intrinsic Pulsatile Gonadotropin-Releasing Hormone Secretion Is Regulated by the Expression of Cyclic Nucleotide-Gated Channels in GT1 Cells Endocrinology, July 1, 2007; 148(7): 3299 - 3306. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. E. Gonzalez-Iglesias, Y. Jiang, M. Tomic, K. Kretschmannova, S. A. Andric, H. Zemkova, and S. S. Stojilkovic Dependence of Electrical Activity and Calcium Influx-Controlled Prolactin Release on Adenylyl Cyclase Signaling Pathway in Pituitary Lactotrophs Mol. Endocrinol., September 1, 2006; 20(9): 2231 - 2246. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Gomez, S. E. la Fleur, R. I. Weiner, M. F. Dallman, and M. El Majdoubi Decreased Gonadotropin-Releasing Hormone Neuronal Activity Is Associated with Decreased Fertility and Dysregulation of Food Intake in the Female GPR-4 Transgenic Rat Endocrinology, September 1, 2005; 146(9): 3800 - 3808. [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 |
