Prenatal Nicotine Exposure Impairs Executive Control Signals in Medial Prefrontal Cortex
Prenatal Nicotine Exposure Impairs Executive Control Signals in Medial Prefrontal Cortex
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DOI：
10.1038/npp.2015.197
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发表时间：
2016-02-01
影响因子：
7.6
通讯作者：
Roesch, Matthew R.
中科院分区：
文献类型：
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作者：
Bryden, Daniel W.;Burton, Amanda C.;Roesch, Matthew R.
产前尼古丁暴露（PNE）与许多精神疾病有关，包括注意力缺陷多动障碍（ADHD）。目前的文献表明，在ADHD中观察到的核心缺陷反映了由前额叶皮层控制的异常抑制控制。然而，目前还不清楚内侧前额叶皮层（mPFC）的神经活动是如何调制的任务，评估反应抑制或这些神经相关，沿着的行为，受到PNE的影响。为了解决这个问题，我们记录了单个mPFC神经元在控制和PNE大鼠，因为他们执行停止信号任务。我们发现，PNE大鼠在所有试验类型中都更快，做出更多的过早反应，并且不太可能抑制“STOP”试验中的行为，在此期间，大鼠必须抑制已经启动的反应。活动在mPFC调制的反应方向和正相关的准确性和运动时间的控制，但不PNE大鼠。虽然PNE显著减少了与反应方向相关的单个神经元的数量，但在一般STOP试验中观察到的神经活动在很大程度上不受影响。然而，戏剧性的行为赤字停止试验后立即在PNE组的非冲突（GO）试验似乎是介导的冲突监测信号在mPFC的损失。我们的结论是，产前尼古丁暴露使大鼠冲动和破坏发射的mPFC神经元，进行相关的反应方向和冲突监测的信号。
Prenatal nicotine exposure (PNE) is linked to numerous psychiatric disorders including attention deficit hyperactivity disorder (ADHD). Current literature suggests that core deficits observed in ADHD reflect abnormal inhibitory control governed by the prefrontal cortex. Yet, it is unclear how neural activity in the medial prefrontal cortex (mPFC) is modulated during tasks that assess response inhibition or if these neural correlates, along with behavior, are affected by PNE. To address this issue, we recorded from single mPFC neurons in control and PNE rats as they performed a stop-signal task. We found that PNE rats were faster for all trial-types, made more premature responses, and were less likely to inhibit behavior on 'STOP' trials during which rats had to inhibit an already initiated response. Activity in mPFC was modulated by response direction and was positively correlated with accuracy and movement time in control but not PNE rats. Although the number of single neurons correlated with response direction was significantly reduced by PNE, neural activity observed on general STOP trials was largely unaffected. However, dramatic behavioral deficits on STOP trials immediately following non-conflicting (GO) trials in the PNE group appear to be mediated by the loss of conflict monitoring signals in mPFC. We conclude that prenatal nicotine exposure makes rats impulsive and disrupts firing of mPFC neurons that carry signals related to response direction and conflict monitoring.