Sensorimotor gating and schizophrenia. Human and animal model studies.
Sensorimotor gating and schizophrenia. Human and animal model studies.
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DOI：
10.1001/archpsyc.1990.01810140081011
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发表时间：
1990-02
影响因子：
--
通讯作者：
D. Braff;M. Geyer
中科院分区：
文献类型：
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作者：
D. Braff;M. Geyer
感觉运动门控的人类和动物模型研究使我们能够了解精神分裂症患者注意力异常和单胺能改变的功能意义。临床上，精神分裂症患者报告对感觉刺激过度敏感，理论上与刺激过载相关，并导致认知碎片化。使用皮层事件相关电位和惊吓反应的前脉冲抑制的范例表明，精神分裂症患者也有受损的中枢神经系统抑制（感觉运动门控）。动物模型研究表明，增加全身胺能活性和增加的多巴胺神经核张力导致感觉运动门控失败，类似于精神分裂症患者中所见。所观察到的精神分裂症和动物模型缺陷的时间过程与单胺能神经元功能的“时间图”（即几百毫秒）是一致的。感觉运动门控的研究使研究人员能够对精神分裂症疾病谱中神经元的空间和时间映射、特质和状态缺陷以及脆弱性因素进行评论。通过将注意力理论转化为可检验的假设，精神分裂症的神经生物学变得更加清晰。
Human and animal model studies of sensorimotor gating allow us to understand the functional significance of attentional abnormalities and monoaminergic alterations in patients with schizophrenic disorders. Clinically, schizophrenic patients report oversensitivity to sensory stimulation that theoretically correlates with stimulus overload and leads to cognitive fragmentation. Paradigms using cortical event-related potentials and the prepulse inhibition of startle responses show that schizophrenic patients also have impaired central nervous system inhibition (sensorimotor gating). Animal model studies demonstrate that increased systemic aminergic activity and increased nucleus accumbens dopamine tone causes sensorimotor gating failure, similar to that seen in schizophrenic patients. The time course of the observed schizophrenic and animal model deficits is compatible with the "temporal map" of monoaminergic neuron functions (le, several hundred milliseconds). Studies of sensorimotor gating allow investigators to comment on the spatial and temporal mapping of neurons, trait and state deficits, and vulnerability factors in the schizophrenic spectrum of disorders. By translating attentional theories into testable hypotheses, the neurobiology of schizophrenic disorders becomes clearer.