WordNet

extreme depression characterized by tearful sadness and irrational fears
a concavity in a surface produced by pressing; "he left the impression of his fingers in the soft mud" (同)impression, imprint
a long-term economic state characterized by unemployment and low prices and low levels of trade and investment (同)slump, economic crisis
a mental state characterized by a pessimistic sense of inadequacy and a despondent lack of activity
angular distance below the horizon (especially of a celestial object)
pushing down; "depression of the space bar on the typewriter"
sad feelings of gloom and inadequacy
of or resembling an endogen
derived or originating internally (同)endogenic
a period during the 1930s when there was a worldwide economic depression and mass unemployment (同)Great_Depression

PrepTutorEJDIC

憂うつ病,うつ病
〈C〉『くぼ地』,くぼみ / 〈U〉〈C〉『意気消沈』,憂うつ;うつ病 / 〈C〉『不景気』,不況 / 〈U〉押し下げること,降下,低下
(生物が)内部から成長する,内性の,内因性の

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/02/22 00:14:05」(JST)

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Endogenous Depression is an atypical sub-class of the Mood Disorder, Clinical Depression (A.K.A. Major Depressive Disorder). Endogenous Depression includes patients with treatment-refractory, unipolar, non-psychotic, Major Depressive Disorder, characterized by a dysregulation of the Endogenous Opioid System and not of the Monoaminergic System. Patients who fall in this sub-class typically respond very well to synthetic opioids which act on the μ-opioid receptors and thought to result in increased serotonin production and norepinephrine reuptake inhibition, including Tramadol, Tapentadol, Buprenorphine, and other similar, synthetic, atypical, opioid analgesics. However, due to the addictive qualities and "taboo" nature opioids have in the eyes of the general public, doctors have been reluctant to delve into research on or treatments for Endogenous Depression, and therefore, patients who suffer the condition usually go untreated.^[1]^[2]

It is also thought that Endogenous Depression is a mood disorder that affects some people from birth and is believed to be a genetic condition. A sufferer is prone to become depressed on the advent of traumatic events, exhaustion or when under high levels of stress and may not be aware of the disorder until confronted by symptoms of depression for the first time.

Depressive episodes can occur at any age, but despite the predisposition may never become a serious problem. The severity of depression resulting from a diagnosis can vary greatly, from mild to severe. Worsening of a persons mood may not be triggered by any external element. It is hard to determine its endogenous origin. It is often the case that a sufferer first confronted with life events that might trigger depressive condition and when no particular source of the mood disorder is found, the depression is considered to be endogenous.

History

Endogenous Depression was initially considered valuable as a means of diagnostic differentiation with Reactive depression. While the latter's onset could be attributed to adverse life events and treated with talk therapy, the former would indicate treatment with antidepressants.^[3] Indeed, this view of endogenous depression is at the root of the popular view that mood disorders are a reflection of a 'chemical imbalance' in the brain. More recent research has shown that the probability of an endogenous depression patient experiencing an adverse life event prior to a depressive episode is roughly the same as for a Reactive depression patient and the efficacy of antidepressant therapy bears no statistical correlation with the patient's diagnostic classification along this axis.^[4]

References

^ "Does the antidepressive response to opiate treatment describe a subtype of depression?". European Neuropsychopharmacology. 4 16. 2006.
^ Bodkin, JA; Zornberg, GL, Lukas, SE, Cole, JO (February 1995). "Harvard Medical School Clinical Study "Buprenorphine treatment of refractory depression."". Journal of Clinical Psychopharmacology 15 (1): 49–57. doi:10.1097/00004714-199502000-00008. PMID 7714228.
^ Kramer, T (2002). "Endogenous Versus Exogenous: Still Not the Issue". Medscape Psychopharmacology Today. 7 1.
^ Watkins, JT; Leber WR, Imber SD, Collins JF, Elkin I, Pilkonis PA, Sotsky SM, Shea MT, Glass DR (1993). "Temporal Course Of Change Of Depression". Journal of Consulting & Clinical Psychology. 5 61 (858): 64.

External links

Classification of depression on NetDoctor
Endogenous Depression Information
Endogenous Depression Help Resources

Psychiatry portal

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1. 成人における単極性うつ病：疫学、病因、および神経生物学 unipolar depression in adults epidemiology pathogenesis and neurobiology
2. 急速交代性の双極性障害：疫学、病因、臨床的特徴、および診断 rapid cycling bipolar disorder epidemiology pathogenesis clinical features and diagnosis
3. 成人における単極性うつ病：予後および経過 unipolar depression in adults prognosis and course of illness
4. 成人における単極性うつ病：経頭蓋磁気刺激（TMS）による治療 unipolar depression in adults treatment with transcranial magnetic stimulation tms
5. 成人における単極性うつ病：ニューロモデュレーション治療の概要 unipolar depression in adults overview of neuromodulation procedures

English Journal

5-HT(1B) mRNA expression after chronic social stress.

Furay AR, McDevitt RA, Miczek KA, Neumaier JF.SourceDepartment of Psychiatry and Behavioral Sciences, University of Washington, Harborview Medical Center, 300 9th Avenue, Room 313, Box 359911, Seattle, WA 98104, USA.
Behavioural brain research.Behav Brain Res.2011 Oct 31;224(2):350-7. Epub 2011 Jun 21.
Chronic stress contributes to vulnerability for depression and drug addiction. The function of the serotonergic system has been found to be modified by chronic stress and these changes may play an important role in stress-related relapses to drug craving. The 5-HT(1B) receptor is expressed in nucleu
PMID 21718722

Involvement of AMPA receptor in both the rapid and sustained antidepressant-like effects of ketamine in animal models of depression.

Koike H, Iijima M, Chaki S.SourceDiscovery Pharmacology, Molecular Function and Pharmacology Laboratories, Taisho Pharmaceutical Co., Ltd., 1-403 Yoshino-cho, Kita-ku, Saitama, Saitama 331-9530, Japan.
Behavioural brain research.Behav Brain Res.2011 Oct 10;224(1):107-11. Epub 2011 Jun 6.
A growing body of evidence has suggested that the dysfunction of glutamatergic systems plays a pivotal role in major depressive disorder (MDD). In clinical studies, an N-methyl-d-aspartate receptor antagonist, ketamine, was shown to exert both rapid and sustained antidepressant effects in patients w
PMID 21669235