Cellular Mechanisms of Infralimbic and Prelimbic Prefrontal Cortical Inhibition and Dopaminergic Modulation of Basolateral Amygdala Neurons In Vivo
Cellular Mechanisms of Infralimbic and Prelimbic Prefrontal Cortical Inhibition and Dopaminergic Modulation of Basolateral Amygdala Neurons In Vivo
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DOI：
10.1523/jneurosci.22-01-00324.2002
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发表时间：
2002-01
期刊：
影响因子：
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通讯作者：
J. Rosenkranz;A. Grace;Mh;J. A. R. We;Nicole Macmurdo;Christine A. Wyant;B. Lowry
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文献类型：
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作者：
J. Rosenkranz;A. Grace;Mh;J. A. R. We;Nicole Macmurdo;Christine A. Wyant;B. Lowry
基底外侧杏仁核（BLA）被认为与精神分裂症，抑郁症和其他显示情感成分的疾病有关。BLA的神经元活动和BLA介导的情感行为由部分从感觉关联皮层区域传输的感觉刺激驱动。这些相同的行为可能是由前额叶皮质（PFC）输入BLA调节。然而，目前尚不清楚两组BLA的PFC输入如何对BLA介导的行为施加相反的作用;具体地说，目前还不清楚PFC输入如何对BLA投射神经元施加抑制作用。多巴胺（DA）受体活化增强了BLA介导的行为。虽然我们已经证明，DA抑制内侧PFC输入的BLA和增强感觉皮层的输入，其行动的精确的细胞机制是未知的。在这项研究中，我们usein体内细胞内记录，以确定的手段，从PFC抑制BLA投射神经元，对比，从关联感觉皮层（Te 3），驱动BLA投射神经元，DA受体激活神经元的兴奋性，自发突触后电位（PSP），和PFC诱发的PSP的DA受体激活的影响。我们发现，PFC刺激抑制BLA投射神经元的三种机制：氯离子介导的超极化，神经元输入电阻的持续下降，分流的PSP，所有的影响可能是由于招聘的抑制性中间神经元。DA受体激活通过突触后机制（通过DA D2受体）增强神经元输入阻力，抑制自发发生和PFC诱发的PSP（通过DA D1受体），并增强Te 3诱发的PSP。
The basolateral amygdala (BLA) is believed to be involved in schizophrenia, depression, and other disorders that display affective components. The neuronal activity of the BLA, and BLA-mediated affective behaviors, are driven by sensory stimuli transmitted in part from sensory association cortical regions. These same behaviors may be regulated by prefrontal cortical (PFC) inputs to the BLA. However, it is unclear how two sets of glutamatergic inputs to the BLA can impose opposing actions on BLA-mediated behaviors; specifically, it is unclear how PFC inputs exert inhibitory actions over BLA projection neurons. Dopamine (DA) receptor activation enhances BLA-mediated behaviors. Although we have demonstrated that DA suppresses medial PFC inputs to the BLA and enhances sensory cortical inputs, the precise cellular mechanisms for its actions are unknown. In this study we usein vivo intracellular recordings to determine the means by which glutamatergic inputs from the PFC inhibit BLA projection neurons, contrast that with glutamatergic inputs from the association sensory cortex (Te3) that drive BLA projection neurons, and examine the effects of DA receptor activation on neuronal excitability, spontaneous postsynaptic potentials (PSPs), and PFC-evoked PSPs. We found that PFC stimulation inhibits BLA projection neurons by three mechanisms: chloride-mediated hyperpolarization, a persistent decrease in neuronal input resistance, and shunting of PSPs; all effects are possibly attributable to recruitment of inhibitory interneurons. DA receptor activation enhanced neuronal input resistance by a postsynaptic mechanism (via DA D2 receptors), suppressed spontaneously occurring and PFC-evoked PSPs (via DA D1 receptors), and enhanced Te3-evoked PSPs.