Flach K A, Adler L E, Gerhardt G A, Miller C, Bickford P, MacGregor R J
University of Colorado, Department of Aerospace Engineering, Boulder, USA.
Biol Psychiatry. 1996 Dec 15;40(12):1230-45. doi: 10.1016/0006-3223(95)00624-9.
We have developed a unique computer model of the CA3 region of the hippocampus that simulates the P50 auditory evoked potential response to repeated stimuli in order to study the neuronal circuits involved in a sensory processing deficit associated with schizophrenia. Our computer model of the CA3 hippocampal network includes recurrent activation from within the CA3 region as well as input from the entorhinal cortex and the medial septal nucleus. We used the model to help us determine if the cortical and septal inputs to the CA3 hippocampus alone are responsible for the gating of auditory evoked activity, or if the strong recurrent activity within the CA3 region contributes to this phenomenon. The model suggests that the medial septal input is critical for normal gating; however, to a large extent the activity of the medial septal input can be replaced by simulated stimulation of the hippocampal neurons by a nicotinic agonist. The model is thus consistent with experimental data that show that nicotine restores gating of the N40 evoked potential in fimbria-fornix lesioned rats and of the P50 evoked potential in schizophrenic patients.
我们开发了一种独特的海马体CA3区计算机模型，该模型模拟对重复刺激的P50听觉诱发电位反应，以研究与精神分裂症相关的感觉处理缺陷中涉及的神经回路。我们的CA3海马体网络计算机模型包括CA3区域内的反复激活以及来自内嗅皮质和内侧隔核的输入。我们使用该模型来帮助确定仅CA3海马体的皮质和隔区输入是否负责听觉诱发活动的门控，或者CA3区域内强烈的反复活动是否促成了这一现象。该模型表明内侧隔区输入对正常门控至关重要；然而，在很大程度上，内侧隔区输入的活动可以被烟碱激动剂对海马神经元的模拟刺激所取代。因此，该模型与实验数据一致，实验数据表明尼古丁可恢复穹窿海马伞损伤大鼠的N40诱发电位门控以及精神分裂症患者的P50诱发电位门控。
