Microstimulation reveals opposing influences of prelimbic and infralimbic cortex on the expression of conditioned fear.

Microstimulation reveals opposing influences of prelimbic and infralimbic cortex on the expression of conditioned fear.
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DOI:
10.1101/lm.306106
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发表时间:
2006-11
期刊:
影响因子:
2
通讯作者:
Ivan Vidal-Gonzalez;Benjamín Vidal-Gonzalez;S. Rauch;G. Quirk
Ivan Vidal-Gonzalez;Benjamín Vidal-Gonzalez;S. Rauch;G. Quirk
中科院分区:
医学4区
文献类型:
--
作者:
Ivan Vidal-Gonzalez;Benjamín Vidal-Gonzalez;S. Rauch;G. Quirk

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最近使用损毁、灌流和单位记录技术的研究表明,内侧前额叶皮质(MPFC)的下缘(IL)亚区对于抑制消退后的条件性恐惧是必要的。短暂的IL微刺激与条件性音调配对,旨在模仿神经元的音调反应,减少对音调的条件性恐惧的表达。在本研究中,我们使用微刺激来研究额外的mPFC亚区:前扣带回(PL)、背侧前扣带回(ACD)和中央前内侧皮质(PrCm)在条件性恐惧的表达和消退中的作用。这些都是音调反应区域,与条件性恐惧的获得和消退有关。与IL相反,微刺激PL增加了条件性恐惧的表达,并防止了消亡。微刺激ACD和PrCm则不起作用。在低足电击条件下(避免冰冻的上限水平),微刺激PL和IL的作用相反,分别增加和减少冰冻对条件音的影响。我们认为,PL兴奋杏仁核的输出,而IL抑制杏仁核的输出,为恐惧表达的双向调节提供了一种机制。
Recent studies using lesion, infusion, and unit-recording techniques suggest that the infralimbic (IL) subregion of medial prefrontal cortex (mPFC) is necessary for the inhibition of conditioned fear following extinction. Brief microstimulation of IL paired with conditioned tones, designed to mimic neuronal tone responses, reduces the expression of conditioned fear to the tone. In the present study we used microstimulation to investigate the role of additional mPFC subregions: the prelimbic (PL), dorsal anterior cingulate (ACd), and medial precentral (PrCm) cortices in the expression and extinction of conditioned fear. These are tone-responsive areas that have been implicated in both acquisition and extinction of conditioned fear. In contrast to IL, microstimulation of PL increased the expression of conditioned fear and prevented extinction. Microstimulation of ACd and PrCm had no effect. Under low-footshock conditions (to avoid ceiling levels of freezing), microstimulation of PL and IL had opposite effects, respectively increasing and decreasing freezing to the conditioned tone. We suggest that PL excites amygdala output and IL inhibits amygdala output, providing a mechanism for bidirectional modulation of fear expression.