Abstract
Corticotropin-releasing factor (CRF), a 41 amino acid-containing neuropeptide, acts both as a hypothalamic releasing factor, controlling ACTH and corticosteroid secretion, and at extrahypothalamic CNS sites to modulate mammalian organisms' responses to stress. In this article, the evidence that CRF-containing neurons within the CNS are hyperactive in patients with depression is reviewed. The evidence, taken together, suggests that during depressive episodes, CRF is hypersecreted, resulting in both pituitary-adrenal axis hyperactivity and certain of the signs and symptoms of depression, including decreased appetite, decreased libido and disturbed sleep. There is also evidence that treatments for depression, including antidepressant medications and electroconvulsive therapy, reduce CRF hypersecretion within the CNS. Finally, evidence suggests that alterations in CRF-containing neurons and receptors are responsible for the widely held observation that early untoward life events increase an individual's vulnerability for affective disorders. These findings have a number of implications for treatment of the mood disorders, including the suggestion that the pharmacological manipulation of CRF receptors may provide a novel avenue for the treatment of depression.
| Original language | English |
|---|---|
| Pages (from-to) | 186-194 |
| Number of pages | 9 |
| Journal | Neuroscientist |
| Volume | 3 |
| Issue number | 3 |
| State | Published - May 1 1997 |
| Externally published | Yes |
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Keywords
- Affective disorders
- Antidepressants
- Depression
- Hypothalamic-pituitary-adrenal axis
- Neuroendocrinology
- Stress
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Corticotropin-releasing factor, stress, and depression. / Heit, Stacey; Owens, Michael J.; Plotsky, Paul; Nemeroff, Charles.
In: Neuroscientist, Vol. 3, No. 3, 01.05.1997, p. 186-194.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Corticotropin-releasing factor, stress, and depression
AU - Heit, Stacey
AU - Owens, Michael J.
AU - Plotsky, Paul
AU - Nemeroff, Charles
PY - 1997/5/1
Y1 - 1997/5/1
N2 - Corticotropin-releasing factor (CRF), a 41 amino acid-containing neuropeptide, acts both as a hypothalamic releasing factor, controlling ACTH and corticosteroid secretion, and at extrahypothalamic CNS sites to modulate mammalian organisms' responses to stress. In this article, the evidence that CRF-containing neurons within the CNS are hyperactive in patients with depression is reviewed. The evidence, taken together, suggests that during depressive episodes, CRF is hypersecreted, resulting in both pituitary-adrenal axis hyperactivity and certain of the signs and symptoms of depression, including decreased appetite, decreased libido and disturbed sleep. There is also evidence that treatments for depression, including antidepressant medications and electroconvulsive therapy, reduce CRF hypersecretion within the CNS. Finally, evidence suggests that alterations in CRF-containing neurons and receptors are responsible for the widely held observation that early untoward life events increase an individual's vulnerability for affective disorders. These findings have a number of implications for treatment of the mood disorders, including the suggestion that the pharmacological manipulation of CRF receptors may provide a novel avenue for the treatment of depression.
AB - Corticotropin-releasing factor (CRF), a 41 amino acid-containing neuropeptide, acts both as a hypothalamic releasing factor, controlling ACTH and corticosteroid secretion, and at extrahypothalamic CNS sites to modulate mammalian organisms' responses to stress. In this article, the evidence that CRF-containing neurons within the CNS are hyperactive in patients with depression is reviewed. The evidence, taken together, suggests that during depressive episodes, CRF is hypersecreted, resulting in both pituitary-adrenal axis hyperactivity and certain of the signs and symptoms of depression, including decreased appetite, decreased libido and disturbed sleep. There is also evidence that treatments for depression, including antidepressant medications and electroconvulsive therapy, reduce CRF hypersecretion within the CNS. Finally, evidence suggests that alterations in CRF-containing neurons and receptors are responsible for the widely held observation that early untoward life events increase an individual's vulnerability for affective disorders. These findings have a number of implications for treatment of the mood disorders, including the suggestion that the pharmacological manipulation of CRF receptors may provide a novel avenue for the treatment of depression.
KW - Affective disorders
KW - Antidepressants
KW - Depression
KW - Hypothalamic-pituitary-adrenal axis
KW - Neuroendocrinology
KW - Stress
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UR - http://www.scopus.com/inward/citedby.url?scp=3042986312&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:3042986312
VL - 3
SP - 186
EP - 194
JO - Neuroscientist
JF - Neuroscientist
SN - 1073-8584
IS - 3
ER -