Restuccia D, Valeriani M, Grassi E, Gentili G, Mazza S, Tonali P, Mauguière F
Department of Neurology, Catholic University, Policlinico A. Gemelli, L.go A. 00168 Rome, Italy.
Clin Neurophysiol. 2002 May;113(5):656-71. doi: 10.1016/s1388-2457(02)00034-2.
To determine whether conventional as well as high-frequency somatosensory evoked potentials (SEPs) to upper limb stimulation are influenced by GABAergic intracortical circuitry.
We recorded SEPs from 6 healthy volunteers before and after a single-oral administration of tiagabine. Conventional low-frequency SEPs have been obtained after stimulation of the median nerve, as well as after stimulation of the first phalanx of the thumb, which selectively involves cutaneous finger inputs. Median nerve SEPs have been further analyzed after digital narrow-bandpass filtering, to selectively examine high-frequency responses. Lastly, in order to explain scalp SEP distribution before and after tiagabine administration, we performed the brain electrical source analysis (BESA) of raw data.
After tiagabine administration, conventional scalp SEPs showed a significant amplitude increase of parietal P24, frontal N24 and central P22 components. Similarly, BESA showed a significant strength increase of the second peak of activation of the first two perirolandic dipoles, which are likely to correspond to the N24/P24 and P22 generators. By contrast, no significant changes of high-frequency SEPs were induced by drug intake.
Our findings support the view that both N24/P24 and P22 SEP components are probably generated by deep spiny cell hyperpolarization, which is strongly increased by inhibitory inputs from GABAergic interneurons. By considering the clear influence of inhibitory circuitry in shaping these SEP components, conventional scalp SEP recording could be useful in the functional assessment of the somatosensory cortex in different physiological and pathological conditions. By contrast, intrinsic firing properties of the cell population generating high-frequency SEP responses are unaffected by the increase of recurrent GABAergic inhibition.
确定上肢刺激诱发的传统及高频体感诱发电位(SEP)是否受GABA能皮质内神经回路的影响。
我们记录了6名健康志愿者单次口服噻加宾前后的SEP。在刺激正中神经以及刺激拇指第一指骨(选择性涉及手指皮肤输入)后获得传统低频SEP。在数字窄带滤波后对正中神经SEP进行进一步分析,以选择性检查高频反应。最后,为了解释噻加宾给药前后头皮SEP的分布情况,我们对原始数据进行了脑电源分析(BESA)。
服用噻加宾后,传统头皮SEP显示顶叶P24、额叶N24和中央P22成分的波幅显著增加。同样,BESA显示前两个中央沟周围偶极子激活的第二个峰值强度显著增加,这可能对应于N24/P24和P22的发生器。相比之下,药物摄入未引起高频SEP的显著变化。
我们的研究结果支持以下观点,即N24/P24和P22 SEP成分可能由深层棘状细胞超极化产生,而GABA能中间神经元的抑制性输入会使其强烈增加。考虑到抑制性神经回路对这些SEP成分形成的明显影响,传统头皮SEP记录可能有助于在不同生理和病理条件下对体感皮层进行功能评估。相比之下,产生高频SEP反应的细胞群的内在放电特性不受反复性GABA能抑制增加的影响。