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dc.contributor.authorScott, Lucinda V
dc.contributor.authorDinan, Timothy G
dc.date.accessioned2012-02-03T15:10:17Z
dc.date.available2012-02-03T15:10:17Z
dc.date.issued2012-02-03T15:10:17Z
dc.identifier.citationJ Affect Disord. 2002 Nov;72(2):113-24.en_GB
dc.identifier.issn0165-0327 (Print)en_GB
dc.identifier.issn0165-0327 (Linking)en_GB
dc.identifier.pmid12200202en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209027
dc.description.abstractHyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis is one of the key biological abnormalities described in major depressive disorder, occurring in 30-50% of depressed subjects. Corticotropin-releasing hormone (CRH) and vasopressin (AVP) are the main regulators of this stress system, with the two neuropeptides acting synergistically in bringing about adrenocorticotropin (ACTH) release from the anterior pituitary and cortisol from the adrenal gland. Based on the demonstration of elevated cerebrospinal fluid levels of CRH in depressives, and other evidence, it has been postulated that excess CRH and the resultant increased HPA forward drive form the basis of neuroendocrine dysregulation in depression. However, there is an accumulating body of evidence to support a significant role for AVP in the regulation of pituitary-adrenal activity in health and also in depressive disorder. This review, based on a Medline search from 1980 to 2001, focuses on the functional neuroanatomy, receptor pharmacology, VP synergism with CRH, and the data from clinical and pre-clinical studies that support an important role for AVP in the pathophysiology of major depression. We suggest that future antidepressants may target the vasopressinergic system.
dc.language.isoengen_GB
dc.subject.meshAdrenocorticotropic Hormone/cerebrospinal fluid/drug effects/metabolismen_GB
dc.subject.meshAntidepressive Agents/*pharmacology/*therapeutic useen_GB
dc.subject.meshCorticotropin-Releasing Hormone/cerebrospinal fluid/drug effects/metabolismen_GB
dc.subject.meshDepressive Disorder, Major/cerebrospinal fluid/*drug therapy/physiopathologyen_GB
dc.subject.meshFluoxetine/*pharmacology/*therapeutic useen_GB
dc.subject.meshHumansen_GB
dc.subject.meshHydrocortisone/metabolismen_GB
dc.subject.meshHypothalamo-Hypophyseal System/drug effects/metabolism/physiopathologyen_GB
dc.subject.meshPituitary-Adrenal System/drug effects/metabolism/physiopathologyen_GB
dc.subject.meshReceptors, Vasopressin/drug effectsen_GB
dc.subject.meshVasopressins/cerebrospinal fluid/*drug effects/*metabolismen_GB
dc.titleVasopressin as a target for antidepressant development: an assessment of the available evidence.en_GB
dc.contributor.departmentDepartment of Psychiatry, Cork University Hospital, Cork, Ireland., lucinda@gofree.indigo.ieen_GB
dc.identifier.journalJournal of affective disordersen_GB
dc.description.provinceMunster
html.description.abstractHyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis is one of the key biological abnormalities described in major depressive disorder, occurring in 30-50% of depressed subjects. Corticotropin-releasing hormone (CRH) and vasopressin (AVP) are the main regulators of this stress system, with the two neuropeptides acting synergistically in bringing about adrenocorticotropin (ACTH) release from the anterior pituitary and cortisol from the adrenal gland. Based on the demonstration of elevated cerebrospinal fluid levels of CRH in depressives, and other evidence, it has been postulated that excess CRH and the resultant increased HPA forward drive form the basis of neuroendocrine dysregulation in depression. However, there is an accumulating body of evidence to support a significant role for AVP in the regulation of pituitary-adrenal activity in health and also in depressive disorder. This review, based on a Medline search from 1980 to 2001, focuses on the functional neuroanatomy, receptor pharmacology, VP synergism with CRH, and the data from clinical and pre-clinical studies that support an important role for AVP in the pathophysiology of major depression. We suggest that future antidepressants may target the vasopressinergic system.


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