Cruz Ana V, Mallet Nicolas, Magill Peter J, Brown Peter, Averbeck Bruno B
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London WC1N 3BG, United Kingdom.
J Neurophysiol. 2009 Aug;102(2):1092-102. doi: 10.1152/jn.00344.2009. Epub 2009 Jun 17.
Dopamine depletion in cortical-basal ganglia circuits in Parkinson's disease (PD) grossly disturbs movement and cognition. Classic models relate Parkinsonian dysfunction to changes in firing rates of basal ganglia neurons. However, disturbances in other dynamics of neural activity are also common. Taking both inappropriate firing rates and other dynamics into account and determining how changes in the properties of these neural circuits that occur during PD impact on information coding are thus imperative. Here, we examined in vivo network dynamics in the external globus pallidus (GPe) of rats before and after chronic dopamine depletion. Dopamine depletion led to decreases in the firing rates of GPe neurons and increases in synchronized network oscillations in the beta frequency (13-30 Hz) band. Using logistic regression models, we determined the combined and separate impacts of these factors on network entropy, a measure of the upper bound of information coding capacity. Importantly, changes in these features in dopamine-depleted rats led to a significant decrease in GPe network entropy. Changes in firing rates had the largest impact on entropy, with changes in synchrony also decreasing entropy at the network level. Changes in autocorrelations tended to offset these effects because autocorrelations decreased entropy more in the control animals. Thus it is possible that reduced information coding capacity within basal ganglia networks may contribute to the behavioral deficits accompanying PD.
帕金森病（PD）中皮质 - 基底神经节回路的多巴胺耗竭严重扰乱运动和认知。经典模型将帕金森氏功能障碍与基底神经节神经元的放电频率变化联系起来。然而，神经活动的其他动力学干扰也很常见。因此，必须同时考虑不适当的放电频率和其他动力学，并确定PD期间这些神经回路特性的变化如何影响信息编码。在这里，我们研究了慢性多巴胺耗竭前后大鼠外侧苍白球（GPe）的体内网络动力学。多巴胺耗竭导致GPe神经元放电频率降低，β频率（13 - 30Hz）波段的同步网络振荡增加。使用逻辑回归模型，我们确定了这些因素对网络熵的综合和单独影响，网络熵是信息编码能力上限的一种度量。重要的是，多巴胺耗竭大鼠中这些特征的变化导致GPe网络熵显著降低。放电频率的变化对熵的影响最大，同步性的变化在网络水平上也降低了熵。自相关的变化倾向于抵消这些影响，因为自相关在对照动物中使熵降低得更多。因此，基底神经节网络内信息编码能力的降低可能导致伴随PD的行为缺陷。
