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The neurobiology of depression-revisiting the serotonin hypothesis. II. Genetic, epigenetic and clinical studies Introduction
被引:62
作者:
Albert, Paul R.
[1
]
Benkelfat, Chawki
[2
,3
]
机构:
[1] Univ Ottawa, Ottawa Hosp Res Inst Neurosci, Ottawa, ON K1H 8M5, Canada
[2] McGill Univ, Dept Psychiat, Montreal, PQ H3A 1A1, Canada
[3] McGill Univ, Dept Neurol & Neurosurg, Montreal, PQ H3A 1A1, Canada
关键词:
serotonin;
depression;
anxiety;
genetics;
epigenetics;
antidepressant;
ANTIDEPRESSANT FLUOXETINE;
NERVE-TERMINALS;
RECEPTOR;
D O I:
10.1098/rstb.2012.0535
中图分类号:
Q [生物科学];
学科分类号:
07 ;
0710 ;
09 ;
摘要:
The serotonin system originates from a small number of neurons (a few hundred thousand of the 100 billion in man) located in the midbrain raphe nuclei, that project widely throughout the central nervous system to influence a large array of inter-related biological functions, not least of which are circuits involved in mood and emotion. The serotonin hypothesis of depression has postulated that a reduction in serotonin leads to increased predisposition to depression. Indeed, it has become evident from therapeutic strategies that affect serotonin activity, that alterations in serotonin may not only predispose to depression, but also to aggressive behaviour, impulsivity, obsessive-compulsive behaviour and suicide. Many potential mechanisms known to alter the genes that regulate the serotonin system, including developmental epigenetic modifications, are presented, as additional evidence implicating the serotonin system. This second issue of two special issues of Philosophical Transactions B presents a series of reviews, perspectives and new findings that argue that the serotonin hypothesis remains an important idea that continues to guide research into the aetiology and treatment of depression.
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