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Submitted on May 6, 2003
Accepted on October 10, 2003
1 Departments of Internal Medicine and Cell Biology, University of Virginia, Charlottesville, VA 22908
* To whom correspondence should be addressed. E-mail: smm4n{at}virginia.edu.
Pulsatile release of gonadotropin-releasing hormone (GnRH) provides central control of reproduction. GnRH neuron activity is likely synchronized to produce hormone pulses, but the mechanisms are largely unknown. One candidate for communication among these neurons is GnRH itself. Cultured embryonic and immortalized GnRH neurons express GnRH receptor type I (GnRHR1), but expression has not been shown in adult GnRH neurons. Using mice that express green fluorescent protein (GFP) in GnRH neurons, we tested if adult GnRH neurons express GnRHR1. GFP-positive (n = 42) and -negative neurons (n = 22) were harvested from brain slices and single cell RT-PCR was performed with cell contents. 52% of the GnRH neurons tested, but only 9% of non-GnRH hypothalamic neurons expressed GnRHR1; no false harvest controls (n = 13) were positive. GnRHR1 expression within GnRH neurons suggested a physiological ultrashort loop feedback role for GnRH. We thus examined the effect of GnRH on the firing rate of GnRH neurons. Low dose GnRH (20 nM) significantly decreased firing rate in 12 of 22 neurons (by 42 ± 4%, P < 0.05), whereas higher doses increased firing rate (200 nM, 5 of 10 72 ± 26%; 2000 nM 9 of 13 53 ± 8%). Interestingly, the fraction of GnRH neurons responding was similar to that in which GnRHR1 was detected. Together these data demonstrate that a subpopulation of GnRH neurons express GnRHR1 and respond to GnRH with altered firing. The dose-dependence suggests this autocrine control of GnRH neurons may be not only a mechanism for generating/modulating pulsatile release, it may also be involved in the switch between pulse and surge modes of release.
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