The role of dorsal third ventricle α2 adrenergic antagonism or glucocorticoid antagonism in modulating the neuroendocrine stress response to acute ozone exposure
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WKYICV-KR2024 Science Hub Mianserin and Mife Manuscript Updated 6.9.25.xlsx
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Complete Metadata
| @type | dcat:Dataset |
|---|---|
| accessLevel | public |
| bureauCode |
[ "020:00" ] |
| contactPoint |
{ "fn": "Katherine Rentschler", "hasEmail": "mailto:rentschler.katherine@epa.gov" } |
| description | Dorsal third ventricle infusions of the alpha 2 adrenergic receptor antagonist, mianserin- which increases brain concentrations of dopamine, serotonin, and acetylcholine, or the glucocorticoid receptor antagonist, mifepristone, were performed in male WKY rats prior to acute ozone exposure at 0.8 ppm for 4 hours. This experiment was designed to target hippocampal and hypothalamic neuromodulation to determine the role of indoleamines, monoamines, and glucocorticoids in mediating the systemic and pulmonary effects to ozone exposure. |
| distribution |
[ { "title": "WKYICV-KR2024 Science Hub Mianserin and Mife Manuscript Updated 6.9.25.xlsx", "mediaType": "application/vnd.openxmlformats-officedocument.spreadsheetml.sheet", "downloadURL": "https://pasteur.epa.gov/uploads/10.23719/1532349/WKYICV-KR2024%20Science%20Hub%20Mianserin%20and%20Mife%20Manuscript%20Updated%206.9.25.xlsx" } ] |
| identifier | https://doi.org/10.23719/1532349 |
| keyword |
[ "Catecholamines", "Ozone", "air pollution", "glucocorticoids", "monoamines", "neuroendocrine stress axes", "pulmonary injury" ] |
| license | https://pasteur.epa.gov/license/sciencehub-license.html |
| modified | 2025-06-09 |
| programCode |
[ "020:000" ] |
| publisher |
{ "name": "U.S. EPA Office of Research and Development (ORD)", "subOrganizationOf": { "name": "U.S. Environmental Protection Agency", "subOrganizationOf": { "name": "U.S. Government" } } } |
| references |
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| rights |
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| title | The role of dorsal third ventricle α2 adrenergic antagonism or glucocorticoid antagonism in modulating the neuroendocrine stress response to acute ozone exposure |