The first theoretical model on the neurophysiological basis of the N400: the deflection reflects layer I dendritic plateaus on a preparatory state of synaptic integration that precedes layer V somatic burst firing for conscious identification of the higher-order features of the stimulus (a late positive shift). Plateaus ensue from apical disinhibition by vasoactive intestinal polypeptide-positive interneurons (VIPs) through suppression of Martinotti cells, opening the gates for glutamatergic feedback to trigger dendritic regenerative potentials. Cholinergic transients contribute to these dynamics directly, holding a central role in the N400 deflection. The stereotypical timing of the (frontal) glutamatergic feedback and the accompanying cholinergic transients account for the enigmatic “invariability” of the peak latency in the face of a gamut of different stimuli and paradigms. The theoretical postulations presented here may bring about unprecedented level of detail for the N400 deflection to be used in the study of schizophrenia, Alzheimer's disease and other higher-order pathologies. The substrates of a late positive component, the Mismatch Negativity and the Semantic Prediction Potentials are also surveyed.

N400 神经生理学基础的第一个理论模型：偏转反映了 I 层树突平台处于突触整合的准备状态，该状态在 V 层躯体爆发放电之前，用于有意识地识别刺激的高阶特征（晚期正转移）。血管活性肠多肽阳性中间神经元 (VIP) 通过抑制 Martinotti 细胞，打开谷氨酸能反馈的大门以触发树突再生潜能，从而导致顶端去抑制而出现平台期。胆碱能瞬变直接影响这些动力学，在 N400 偏转中发挥核心作用。（额叶）谷氨酸能反馈的刻板时间和伴随的胆碱能瞬变解释了面对各种不同刺激和范式时峰值延迟的神秘“不变性”。这里提出的理论假设可能会为 N400 偏转带来前所未有的细节水平，用于研究精神分裂症、阿尔茨海默病和其他高级病理。还调查了晚期正成分的底物、错配负性和语义预测潜力。