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Effect of Steroid Milieu on Gonadotropin-Releasing Hormone-1 Neuron Firing Pattern and Luteinizing Hormone Levels in Male Mice¹

Departments of Internal Medicine and Cell Biology, University of Virginia, Charlottesville, Virginia 22908

ABSTRACT

GnRH neuronal function is regulated by gonadal hormone feedback. In males, testosterone can act directly or be converted to either dihydrotestosterone (DHT) or estradiol (E₂). We examined central steroid feedback by recording firing of green fluorescent protein (GFP)-identified GnRH neurons in brain slices from male mice that were intact, castrated, or castrated and treated with implants containing DHT, E₂, or E₂+DHT. Castration increased LH levels. DHT or E₂ alone partially suppressed LH, whereas E₂+DHT reduced LH to intact levels. Despite the inhibitory actions on LH, the combination of E₂+DHT increased GnRH neuron activity relative to other treatments, reflected in mean firing rate, amplitude of peaks in firing rate, and area under the curve of firing rate vs. time. Cluster8 was used to identify peaks in firing activity that may be correlated with hormone release. Castration increased the frequency of peaks in firing rate. Treatment with DHT failed to reduce frequency of these peaks. In contrast, treatment with E₂ reduced peak frequency to intact levels. The frequency of peaks in firing rate was intermediate in animals treated with E₂+DHT, perhaps suggesting the activating effects of this combination partially counteracts the inhibitory actions of E₂. These data indicate that E₂ mediates central negative feedback in males primarily by affecting the pattern of GnRH neuron activity, and that androgens combined with estrogens have a central activating effect on GnRH neurons. The negative feedback induced by E₂+DHT to restore LH to intact levels may mask an excitatory central effect of this combination.

estradiol, gonadotropin-releasing hormone, luteinizing hormone, steroid hormones

¹ Supported by the National Institute of Child Health and Human Development/National Institutes of Health through cooperative agreement U54HD28934 and the Ligand Assay and Analysis Core. A preliminary report of this work was presented at the 38th annual meeting of the Society for the Study of Reproduction, 24–27 July 2005, Quebec City, Quebec, Canada.

² Correspondence: Suzanne M. Moenter, Department of Internal Medicine, P.O. Box 800578, University of Virginia, Charlottesville, VA 22908. FAX: 434 9820088; smm4n{at}virginia.edu

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