We previously reported anatomical and functional evidence for a direct, inhibitory neural pathway that regulates testosterone (T) secretion independently of the pituitary. This pathway is activated by the intracerebroventricular (icv) administration of agents that stimulate stress responses, such as interleukin 1- (IL-1), corticotrophin releasing factor (CRF) and norepinephrine, which results in a blunted T response to the administration of human chorionic gonadotropin (hCG). Blunting of the T response is mediated by central -adrenergic receptor stimulation. CRF, but not ethanol or IL-1 acts directly on the paraventricular nucleus (PVN) of the hypothalamus to activate the pathway. Here we explored the role played by brain areas hypothesized to be part of this pathway, such as neurons in the dorsal pons [including the locus coeruleus (LC) of the brain stem], where norepinephrine is produced. Microinfusion of ethanol or IL-1, but not CRF, into these neurons activated the pathway. Electrolytic lesions of this region significantly reversed the inhibitory effect of icv-administered ethanol on hCG-induced T release, while having no effect on the ability of IL-1 or CRF to do so. However, the icv administration of IL-1, ethanol or CRF, in doses that rapidly inhibit the T response to hCG, all caused a significant depletion of norepinephrine from the LC. Collectively, these results indicate that in addition to the PVN, the brain stem area containing the LC is part of a neural pathway that connects the brain to the testes independently of the pituitary. We also speculate that ethanol may stimulate this pathway through NE-dependent activation of the dorsal pons.