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Submitted on July 13, 2005
Accepted on October 3, 2005
The Clayton Foundation Laboratories for Peptide Biology, The Salk Institute, 10010 N. Torrey Pines Road, La Jolla, CA 92037
* To whom correspondence should be addressed. E-mail: crivier{at}salk.edu.
Activation of a neural brain-testicular pathway by the intracerebroventricular (icv) injection of the 
-adrenergic agonist isoproterenol (ISO), the hypothalamic peptide corticotropin-releasing factor (CRF) or alcohol (EtOH), rapidly decreases the testosterone (T) response to human chorionic gonadotropin (hCG). To elucidate the intratesticular mechanisms responsible for this phenomenon, we investigated the influence of icv-injected ISO, CRF or EtOH on levels of the steroidogenic acute regulatory (StAR) protein, the peripheral-type benzodiazepine receptor (PBR) and the cytochrome P450 side-chain cleavage enzyme (P450scc) in semi-purified Leydig cells. ISO (10 µg), CRF (5 µg) or EtOH (5 µl of 200 proof, a dose that does not induce neuronal damage nor leaks to the periphery) rapidly decreased StAR and PBR, but not P450scc protein levels. Levels of the variant of the neuronal nitric oxide (NO) synthase (NOS) that is restricted to Leydig cells, TnNOS, significantly increased in response to ISO, CRF and EtOH over the time-course of altered StAR/PBR concentrations. However, pretreatment of the rats with Nwnitro-arginine methylester (L-NAME), which blocked ISO-induced increases in TnNOS, neither restored the T response to hCG nor prevented the decreases in StAR and PBR. These results provide evidence of concomitant changes in Leydig cell StAR and PBR levels in live rats. They also indicate that activation of a neural brain-testicular pathway rapidly decreases concentrations of these steroidogenic proteins while upregulating testicular NO production. However, further studies are necessary to elucidate the functional role played by this gas in our model.
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