Department of Psychology, University of California, Los Angeles, Los Angeles, CA 90095-1563, USA.
Psychophysiology. 2011 Apr;48(4):470-8. doi: 10.1111/j.1469-8986.2010.01119.x. Epub 2010 Aug 23.
Although malfunctioning of inhibitory processes is proposed as a pathophysiological mechanism in schizophrenia and has been studied extensively with the P50 gating paradigm, the brain regions involved in generating and suppressing the P50 remain unclear. The current investigation used EEG source analysis and the standard S1-S2 paradigm to clarify the neural structures associated with P50 gating in 16 schizophrenia patients and 14 healthy subjects. Based on prior research, the superior temporal gyrus, hippocampus, dorsolateral prefrontal cortex, thalamus, and their dipole moments were evaluated. In modeling the P50, a neural network involving all four brain regions provided the best goodness-of-fit across both groups. In healthy subjects, the P50 ratio score correlated positively with the hippocampal dipole moment ratio, whereas a significant association with the DLPFC dipole moment ratio was observed in schizophrenia patients. In each instance, the neural structure was found to account for unique variance in explaining the P50 ratio, along with some suggestion of DLPFC involvement in healthy subjects.
虽然抑制过程的功能障碍被认为是精神分裂症的一种病理生理机制，并已通过 P50 门控范式进行了广泛研究，但产生和抑制 P50 的大脑区域仍不清楚。本研究使用 EEG 源分析和标准 S1-S2 范式，以明确与 16 名精神分裂症患者和 14 名健康受试者的 P50 门控相关的神经结构。基于先前的研究，评估了颞上回、海马体、背外侧前额叶皮质、丘脑及其偶极子。在对 P50 进行建模时，涉及所有四个脑区的神经网络在两组中均提供了最佳的拟合度。在健康受试者中，P50 比值与海马体偶极子比值呈正相关，而在精神分裂症患者中，与 DLPFC 偶极子比值存在显著相关性。在每种情况下，都发现神经结构可以解释 P50 比值的独特方差，同时还表明 DLPFC 在健康受试者中存在参与。
