Department of Psychiatry and Psychotherapy, Georg-August University, Göttingen, Germany.
Eur Arch Psychiatry Clin Neurosci. 2012 Aug;262(5):415-23. doi: 10.1007/s00406-012-0298-7. Epub 2012 Feb 9.
Post-mortem and in vivo studies provide evidence for a link between reduced plasticity and dysconnectivity in schizophrenia patients. It has been suggested that the association between plasticity and connectivity contributes to the pathophysiology and symptomatology of schizophrenia. However, little is known about the impact of glutamate-dependent long-term depression (LTD)-like cortical plasticity on inter-hemispheric connectivity in schizophrenia patients. The aim of the present study was to investigate LTD-like cortical plasticity following excitability-diminishing cathodal transcranial direct current stimulation (tDCS) of the left primary motor cortex (M1) and its effects on the non-stimulated right M1. Eighteen schizophrenia patients and 18 matched (age, gender, handedness, and smoking status) control subjects were investigated in this study. Corticospinal excitability changes following tDCS and intra-cortical inhibitory circuits were monitored with transcranial magnetic stimulation. On the stimulated hemisphere, cathodal tDCS increased resting motor thresholds (RMT) in both groups and decreased motor-evoked potential (MEP) sizes in healthy controls to a greater extent compared to schizophrenia patients. On the non-stimulated hemisphere, RMTs were increased and MEPs were decreased only in the healthy control group. Our results confirm previous findings of reduced LTD-like plasticity in schizophrenia patients and offer hypothetical and indirect in vivo evidence for an association between LTD-like cortical plasticity and inter-hemispheric connectivity in schizophrenia patients. Moreover, our findings highlight the impact of plasticity on connectivity. Dysfunctional N-methyl D-aspartate receptors or modulation of dopaminergic transmission can explain these findings. Nevertheless, the effects of antipsychotic medication still need to be considered.
死后和体内研究为精神分裂症患者中可塑性降低和连接异常之间的联系提供了证据。有人认为，可塑性和连接之间的关联有助于精神分裂症的病理生理学和症状学。然而，对于谷氨酸依赖性长时程抑制（ LTD ）样皮质可塑性对精神分裂症患者大脑半球间连接的影响知之甚少。本研究的目的是探讨左初级运动皮层（ M1 ）兴奋性降低的阴极经颅直流电刺激（ tDCS ）后 LTD 样皮质可塑性及其对未受刺激的右 M1 的影响。本研究共纳入 18 例精神分裂症患者和 18 例匹配的（年龄、性别、利手和吸烟状况）对照组。通过经颅磁刺激监测 tDCS 后的皮质脊髓兴奋性变化和皮质内抑制回路。在受刺激的半球上，阴极 tDCS 增加了两组的静息运动阈值（ RMT ），并且与精神分裂症患者相比，健康对照组的运动诱发电位（ MEP ）大小降低得更明显。在未受刺激的半球上，仅在健康对照组中 RMT 升高，而 MEP 降低。我们的结果证实了先前在精神分裂症患者中存在 LTD 样可塑性降低的发现，并提供了假设的和间接的体内证据，表明精神分裂症患者中 LTD 样皮质可塑性与大脑半球间连接之间存在关联。此外，我们的发现强调了可塑性对连接的影响。功能失调的 N-甲基-D-天冬氨酸受体或多巴胺能传递的调节可以解释这些发现。然而，仍需要考虑抗精神病药物的作用。
