作者: R. Levy , L.-N. Hazrati , M.-T. Herrero , M. Vila , O.-K. Hassani
DOI: 10.1016/S0306-4522(96)00409-5
关键词: Psychology 、 Degenerative disease 、 Subthalamic nucleus 、 Neuroscience 、 Disinhibition 、 Parkinsonism 、 Basal ganglia 、 Parkinson's disease 、 GABAergic 、 Central nervous system
摘要: In the late 1980s, a functional and anatomical model of basal ganglia organization was proposed in order to explain clinical syndrome Parkinson's disease. According this model, pathological overactivity observed subthalamic nucleus output station plays crucial role pathophysiology motor signs The hyperactivity neurons Parkinsonism is viewed as direct consequence hypoactivity external segment pallidum. This article reviews recent data from different experimental approaches that challenge established by reinterpreting interaction between pallidum both normal state. Indeed, neurobiochemical studies have rather unexpectedly shown GABAergic metabolic activities are not decreased human non-human primates with Parkinsonism. absence any decrease activity might be explained functionally antagonistic influences striatal afferences within pallidum, suggested several studies. addition, there clues electrophysiological suggest found may depend solely on level such framework, would explained, at least part, other sources excitation or disinhibition. However, explanation for origin remains speculative.