期刊
JOURNAL OF NEUROSCIENCE
卷 25, 期 32, 页码 7429-7437出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2314-05.2005
关键词
amygdala; medial prefrontal cortex; infralimbic; prelimbic; extinction; fear conditioning
资金
- NIMH NIH HHS [R01 MH066856, R01 MH-066856-01, R01 MH-073610-01, R01 MH073610] Funding Source: Medline
Accumulating evidence indicates that phobic and posttraumatic anxiety disorders likely result from a failure to extinguish fear memories. Extinction normally depends on a new learning that competes with the original fear memory and is driven by medial prefrontal cortex (mPFC) projections to the amygdala. Although mPFC stimulation was reported to inhibit the central medial (CEm) amygdala neurons that mediate fear responses via their brainstem and hypothalamic projections, it is unclear how this inhibition is generated. Because the mPFC has very sparse projections to CEm output neurons, the mPFC-evoked inhibition of the CEm is likely indirect. Thus, this study tested whether it resulted from a feedforward inhibition of basolateral amygdala (BLA) neurons that normally relay sensory inputs to the CEm. However, our results indicate that mPFC inputs excite rather than inhibit BLA neurons, implying that the inhibition of CEm cells is mediated by an active gating mechanism downstream of the BLA.
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