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Submitted on February 21, 2003
Accepted on June 19, 2003
1 Department of Obstetrics Gynecology and Reproductive Sciences, University of California San Francisco, San Francisco, CA 94143, Department of Neurology, University of California Los Angeles, Los Angeles, CA 90095, and Department of Obstetrics and Gynecology, Stanford University, Stanford, CA 94350.
* To whom correspondence should be addressed. 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 if 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 fluorescence 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.
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