期刊
NEUROPSYCHOPHARMACOLOGY
卷 35, 期 1, 页码 105-135出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/npp.2009.109
关键词
amygdala; bed nucleus stria terminalis; startle; CRF; SSRIs; context conditioning
资金
- NIMH [MH069056, MH47840, MH57250, MH59906, 1U19 MH069056]
- Science and Technology Center [IBN-9876754]
- NARSAD Young Investigator award
- American Psychological Association Diversity Program in Neuroscience [5T32 MH18882]
- Intramural Research Program at NIMH
- NATIONAL INSTITUTE OF MENTAL HEALTH [R37MH047840, U19MH069056, ZIAMH002798, R01MH057250, R01MH047840, T32MH018882, R01MH059906] Funding Source: NIH RePORTER
Data will be reviewed using the acoustic startle reflex in rats and humans based on our attempts to operationally define fear vs anxiety. Although the symptoms of fear and anxiety are very similar, they also differ. Fear is a generally adaptive state of apprehension that begins rapidly and dissipates quickly once the threat is removed (phasic fear). Anxiety is elicited by less specific and less predictable threats, or by those that are physically or psychologically more distant. Thus, anxiety is a more long-lasting state of apprehension (sustained fear). Rodent studies suggest that phasic fear is mediated by the amygdala, which sends outputs to the hypothalamus and brainstem to produce symptoms of fear. Sustained fear is also mediated by the amygdala, which releases corticotropin-releasing factor, a stress hormone that acts on receptors in the bed nucleus of the stria terminalis (BNST), a part of the so-called 'extended amygdala.' The amygdala and BNST send outputs to the same hypothalamic and brainstem targets to produce phasic and sustained fear, respectively. In rats, sustained fear is more sensitive to anxiolytic drugs. In humans, symptoms of clinical anxiety are better detected in sustained rather than phasic fear paradigms. Neuropsychopharmacology Reviews (2010) 35, 105-135; doi:10.1038/npp.2009.109; published online 19 August 2009
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