Chang Chun-Hui, Ho Ta-Wen
Institute of Systems Neuroscience, National Tsing Hua University, Hsinchu, Taiwan, 30013.
Department of Life Science, National Tsing Hua University, Hsinchu, Taiwan, 30013.
J Physiol. 2017 Sep 1;595(17):6065-6076. doi: 10.1113/JP274568. Epub 2017 Jul 26.
The basolateral complex of the amygdala (BLA) receives input from the lateral orbitofrontal cortex (lOFC) for cue-outcome contingencies and the medial prefrontal cortex (mPFC) for emotion control. Here we examined how the mPFC modulates lOFC-BLA information flow. We found that the majority of BLA neurons responsive to lOFC stimulation were also responsive to mPFC stimulation. Activation of the mPFC exerted an inhibitory modulation of the lOFC-BLA pathway, which was reversed with intra-amygdala blockade of GABAergic receptors. mPFC tetanus potentiated the lOFC-BLA pathway, but did not alter its inhibitory modulatory gating. These results show that the mPFC potently inhibits lOFC drive of the BLA in a GABA-dependent manner, which is informative in understanding the normal and potential pathophysiological state of emotion and contingency associations in regulating behaviour.
Several neocortical projections converge onto the basolateral complex of the amygdala (BLA), including the lateral orbitofrontal cortex (lOFC) and the medial prefrontal cortex (mPFC). Lateral orbitofrontal input to the BLA is important for cue-outcome contingencies, while medial prefrontal input is essential for emotion control. In this study, we examined how the mPFC, specifically the infralimbic division of the mPFC, modulates lOFC-BLA information flow, using combined in vivo extracellular single-unit recordings and pharmacological manipulations in anaesthetized rats. We found that the majority (over 95%) of BLA neurons that responded to lOFC stimulation also responded to mPFC stimulation. Compared to basal condition, pharmacological (N-methyl-d-aspartate) or electrical activation of the mPFC exerted an inhibitory modulation of the lOFC-BLA pathway, which was reversed with intra-amygdala blockade of GABAergic receptors with combined GABA and GABA antagonists (bicuculline and saclofen). Moreover, mPFC tetanus potentiated the lOFC-BLA pathway, but mPFC tetanus or low-frequency stimulation did not alter its inhibitory modulatory gating on the lOFC-BLA pathway. These results show that the mPFC potently inhibits lOFC drive of BLA neurons in a GABA-dependent manner. Our result is informative in understanding the normal and potential pathophysiological state of emotion and contingency associations regulating behaviour.
杏仁核基底外侧复合体（BLA）接收来自外侧眶额叶皮层（lOFC）的关于线索-结果偶联的输入以及来自内侧前额叶皮层（mPFC）的用于情绪控制的输入。在此，我们研究了mPFC如何调节lOFC-BLA信息流。我们发现，大多数对lOFC刺激有反应的BLA神经元也对mPFC刺激有反应。mPFC的激活对lOFC-BLA通路施加了抑制性调节，而这种调节在杏仁核内阻断GABA能受体后被逆转。mPFC强直刺激增强了lOFC-BLA通路，但并未改变其抑制性调节门控。这些结果表明，mPFC以GABA依赖的方式有力地抑制了BLA的lOFC驱动，这对于理解调节行为时情绪和偶联关联的正常及潜在病理生理状态具有重要意义。
包括外侧眶额叶皮层（lOFC）和内侧前额叶皮层（mPFC）在内的几个新皮层投射汇聚到杏仁核基底外侧复合体（BLA）。BLA的外侧眶额叶输入对于线索-结果偶联很重要，而内侧前额叶输入对于情绪控制至关重要。在本研究中，我们使用麻醉大鼠体内细胞外单单位记录和药理学操作相结合的方法，研究了mPFC，特别是mPFC的下缘区，如何调节lOFC-BLA信息流。我们发现，大多数（超过95%）对lOFC刺激有反应的BLA神经元也对mPFC刺激有反应。与基础状态相比，mPFC的药理学（N-甲基-D-天冬氨酸）或电激活对lOFC-BLA通路施加了抑制性调节，而在杏仁核内用GABA和GABA拮抗剂（荷包牡丹碱和舒氯芬）联合阻断GABA能受体后，这种调节被逆转。此外，mPFC强直刺激增强了lOFC-BLA通路，但mPFC强直刺激或低频刺激并未改变其对lOFC-BLA通路的抑制性调节门控。这些结果表明，mPFC以GABA依赖的方式有力地抑制了BLA神经元的lOFC驱动。我们的结果对于理解调节行为时情绪和偶联关联的正常及潜在病理生理状态具有重要意义。
