Likhtik Ekaterina, Pelletier Joe Guillaume, Paz Rony, Paré Denis
Center for Molecular and Behavioral Neuroscience, Rutgers, The State University of New Jersey, Newark, New Jersey 07102, USA.
J Neurosci. 2005 Aug 10;25(32):7429-37. doi: 10.1523/JNEUROSCI.2314-05.2005.
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.
越来越多的证据表明，恐惧症和创伤后焦虑症可能是由于恐惧记忆未能消退所致。消退通常依赖于一种与原始恐惧记忆相竞争的新学习过程，并且由内侧前额叶皮层（mPFC）向杏仁核的投射所驱动。尽管据报道mPFC刺激可抑制通过其脑干和下丘脑投射介导恐惧反应的中央内侧（CEm）杏仁核神经元，但尚不清楚这种抑制是如何产生的。由于mPFC对CEm输出神经元的投射非常稀疏，mPFC诱发的对CEm的抑制可能是间接的。因此，本研究测试了它是否源于对基底外侧杏仁核（BLA）神经元的前馈抑制，这些神经元通常将感觉输入传递给CEm。然而，我们的结果表明，mPFC输入会兴奋而非抑制BLA神经元，这意味着对CEm细胞的抑制是由BLA下游的一种主动门控机制介导的。
