Major Projects

• Investigation of the mechanisms through which the unstable gases nitric oxide (NO) and carbon monoxide (CO) influence the activity of the HPA axis and participate in its responses to stressors.

  This project combines the use of NO/CO antagonists, the microinfusion of NO/CO donors in select brain areas, and the pharmacological or electrical lesions to study the participation of specific circuitries.
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• Anatomical and functional identification of a novel hypothalamic-testicular pathway that is independent of the pituitary, and through which stress signals within the brain block the ability of Leydig cells to secrete testosterone in response to gonadotropins.

  This project relies on spinal and brain mapping of the proposed pathway by the use of the transynaptic tracer pseudo-rabies virus (PRV). This information is then used to elucidate the participation of the hypothalamic structures that we thus identify, in modulating the effect of brain catecholamines on Leydig cell function. Finally, we plan to investigate the role of this pathway in mediating the ability of specific stressors and/or diseases to decrease testosterone release.
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• Development of a model of rodent prenatal stress that provides a stable anxiety paradigm in adult offspring.

  This project focuses on the investigation of the mechanisms leading to altered HPA axis during mood disorders, using a model of prenatal rodent stress to yield stable measures of anxiety in adult rats.
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• Identification and elucidation of the consequences of fetal alcohol exposure on HPA axis activity in adulthood.

  This project focuses on the mechanisms responsible for the hyperactivity of the HPA axis in adult offspring of dams treated with alcohol during gestation, with special emphasis on hypothalamic and extra-hypothalamic CRF expression, and the role of CRF and its receptors in pathologies associated with prenatal alcohol exposure.
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• Investigation of the mechanisms through which acute or long-term alcohol exposure alters the activity of the HPA axis.

  This project combines in vivo studies (done in rats, wild-type and knockout mice) aimed at elucidating the effect of alcohol on the brain neurocicuitries that impinge on the PVN and on CRF synthesis/release; and in vitro studies (done in primary, immortalized and transfected cells) that investigate the molecular mechanisms through which alcohol alters CRF signal transduction and translation.
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• Investigation of the activity and role of the HPA axis in modulating alcohol self-administration.

  This project focuses on the emergent hypothesis that the HPA axis plays a major role in the transition from controllable alcohol self-administration to addiction, and once addiction is established, in relapse and drug seeking.
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