Bidirectional homeostatic plasticity induced by interneuron cell death and transplantation in vivo

MacKenzie Allen Howard; John L. R. Rubenstein; Scott C. Baraban

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Bidirectional homeostatic plasticity induced by interneuron cell death and transplantation in vivo

机译：Bidirectional homeostatic plasticity induced by interneuron cell death and transplantation in vivo

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Chronic changes in excitability and activity can induce homeostatic plasticity. These perturbations may be associated with neurological disorders, particularly those involving loss or dysfunction of GABA interneurons. In distal-less homeobox 1 (Dlx1~(?/?)) mice with late-onset interneuron loss and reduced inhibition, we observed both excitatory synaptic silencing and decreased intrinsic neuronal excitability. These homeostatic changes do not fully restore normal circuit function, because synaptic silencing results in enhanced potential for long-term potentiation and abnormal gamma oscillations. Transplanting medial ganglionic eminence interneuron progenitors to introduce new GABAergic interneurons, we demonstrate restoration of hippocampal function. Specifically, miniature excitatory postsynaptic currents, input resistance, hippocampal long-termpotentiation, and gamma oscillations are all normalized. Thus, in vivo homeostatic plasticity is a highly dynamic and bidirectional process that responds to changes in inhibition.

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《Proceedings of the National Academy of Sciences of the United States of America》 |2014年第1期|492-497|共6页
作者
MacKenzie Allen Howard; John L. R. Rubenstein; Scott C. Baraban;
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作者单位

Epilepsy Research Laboratory, Department of Neurological Surgery, Department of Psychiatry, University of California, San Francisco, CA 94143;

Nina Ireland Laboratory of Developmental Neurobiology, Department of Psychiatry, University of California, San Francisco, CA 94143;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
中图分类自然科学总论;
关键词
excitatory/inhibitory balance; gamma frequency oscillations; LTP; neural transplantation;

Bidirectional homeostatic plasticity induced by interneuron cell death and transplantation in vivo

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