Jensen O, Goel P, Kopell N, Pohja M, Hari R, Ermentrout B
Brain Research Unit, Low Temperature Laboratory, Helsinki University of Technology, Finland.
Neuroimage. 2005 Jun;26(2):347-55. doi: 10.1016/j.neuroimage.2005.02.008. Epub 2005 Apr 7.
Cortical oscillations in the beta band (13-35 Hz) are known to be modulated by the GABAergic agonist benzodiazepine. To investigate the mechanisms generating the approximately 20-Hz oscillations in the human cortex, we administered benzodiazepines to healthy adults and monitored cortical oscillatory activity by means of magnetoencephalography. Benzodiazepine increased the power and decreased the frequency of beta oscillations over rolandic areas. Minimum current estimates indicated the effect to take place around the hand area of the primary sensorimotor cortex. Given that previous research has identified sources of the beta rhythm in the motor cortex, our results suggest that these same motor-cortex beta sources are modulated by benzodiazepine. To explore the mechanisms underlying the increase in beta power with GABAergic inhibition, we simulated a conductance-based neuronal network comprising excitatory and inhibitory neurons. The model accounts for the increase in the beta power, the widening of the spectral peak, and the slowing down of the rhythms with benzodiazepines, implemented as an increase in GABAergic conductance. We found that an increase in IPSCs onto inhibitory neurons was more important for generating neuronal synchronization in the beta band than an increase in IPSCs onto excitatory pyramidal cells.
已知β波段(13 - 35赫兹)的皮质振荡受γ-氨基丁酸能激动剂苯二氮䓬调节。为了研究人类皮质中产生约20赫兹振荡的机制,我们给健康成年人服用苯二氮䓬,并通过脑磁图监测皮质振荡活动。苯二氮䓬增加了罗兰区β振荡的功率并降低了其频率。最小电流估计表明该效应发生在初级感觉运动皮质的手部区域周围。鉴于先前的研究已确定运动皮质中β节律的来源,我们的结果表明这些相同的运动皮质β源受苯二氮䓬调节。为了探索γ-氨基丁酸能抑制导致β功率增加的潜在机制,我们模拟了一个基于电导的包含兴奋性和抑制性神经元的神经网络。该模型解释了β功率的增加、频谱峰值的拓宽以及苯二氮䓬导致的节律减慢,苯二氮䓬通过增加γ-氨基丁酸能电导来实现。我们发现,抑制性神经元上抑制性突触后电流的增加对于在β波段产生神经元同步比兴奋性锥体细胞上抑制性突触后电流的增加更为重要。