期刊
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
卷 32, 期 7, 页码 1293-1314出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neubiorev.2008.03.006
关键词
Stress; Gene; Strain; Mouse; Inbred; Serotonin; Serotonin transporter; Tryptophan hydroxylase; VMAT2; MAOA; 5-HT1A; 5-HT1B; 5-HT2A; 5-HT2C; 5-HT3; Prefrontal cortex; Hippocampus; Amygdala; Anxiety; Depression; Emergence test; Forced swim test; Restraint
资金
- Intramural NIH HHS [Z01 AA000411-04] Funding Source: Medline
The serotonin system is strongly implicated in the pathophysiology and therapeutic alleviation of stress-related disorders such as anxiety and depression. Serotonergic modulation of the acute response to stress and the adaptation to chronic stress is mediated by a myriad of molecules controlling serotonin neuron development (Pet-1), synthesis (tryptophan hydroxylase I and 2 isozymes), packaging (vesicular monoamine transporter 2), actions at presynaptic and postsynaptic receptors (5-HT1A, 5-HT1B, 5-HT2A, 5-HT2C, 5-HT3A, 5-HT4, 5-HT5A, 5-HT6, 5-HT7), reuptake (serotonin transporter), and degradation (monoamine oxidase A). A growing body of evidence from preclinical rodents models, and especially genetically modified mice and inbred mouse strains, has provided significant insight into how genetic variation in these molecules can affect the development and function of a key neural circuit between the dorsal raphe nucleus, medial prefrontal cortex and amygdala. By extension, such variation is hypothesized to have a major influence on individual differences in the stress response and risk for stress-related disease in humans. The current article provides an update on this rapidly evolving field of research. Published by Elsevier Ltd.
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