Impaired LTD-like motor cortical plasticity in female patients with major depression disorder

Long-term depression (LTD) is a form of physiologic plasticity that is important for reversal learning and may be linked to major depression. Few studies have examined LTP-like plasticity in patients with depression. It is unclear if continuous theta burst stimulation (cTBS) induced LTD is altered i...

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Published inNeuropharmacology Vol. 179; p. 108268
Main Authors Yu, Chang, Li, Ang, Li, Xingxing, Chen, Zan, Wang, Pingjie, Dong, Zhifang, Daskalakis, Zafiris J., Zhou, Dongsheng
Format Journal Article
LanguageEnglish
Published Elsevier Ltd 15.11.2020
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ISSN0028-3908
1873-7064
1873-7064
DOI10.1016/j.neuropharm.2020.108268

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Summary:Long-term depression (LTD) is a form of physiologic plasticity that is important for reversal learning and may be linked to major depression. Few studies have examined LTP-like plasticity in patients with depression. It is unclear if continuous theta burst stimulation (cTBS) induced LTD is altered in depression patients. Here we recruited 29 healthy control subjects and 31 female patients with depression. We performed cTBS protocol on left motor cortex and employed motor evoked potentials (MEPs) response to measure LTD-like plasticity. Peripheral molecules were measured for correlation analyses to cortical plasticity. Our results revealed persistent LTD-like plasticity deficits in female patients with depression. LTD-like plasticity was impaired in patients with depression despite the fact that peripheral concentrations of BDNF were comparable to that of healthy subjects. Conclusions: Our findings provide evidence for impaired LTD-like plasticity in patients with depression which may be an important mechanism linked to the pathophysiology and treatment of this disorder. •Our results revealed persistent LTD-like plasticity deficits in female patients with depression.•LTD-like plasticity was impaired in MDD despite the fact that BDNF were comparable to that of healthy subjects.•Impaired LTD-like plasticity may an important mechanism linked to the pathophysiology and treatment of this disorder.
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ISSN:0028-3908
1873-7064
1873-7064
DOI:10.1016/j.neuropharm.2020.108268