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再探受体运输假说:在已确立的癫痫持续状态期间 AMPA 受体的可塑性。

Receptor trafficking hypothesis revisited: plasticity of AMPA receptors during established status epilepticus.

机构信息

Department of Neurology, University of Virginia, Health Sciences Center, Charlottesville, VA, U.S.A.

出版信息

Epilepsia. 2013 Sep;54 Suppl 6:14-6. doi: 10.1111/epi.12266.

Abstract

Status epilepticus (SE) is associated with a dynamic plasticity of postsynaptic neurotransmitter receptors. The plasticity of AMPA receptor (AMPAR)-mediated glutamatergic transmission during established SE (ESE), after development of benzodiazepine resistance, was evaluated. There was increased frequency and inward rectification of AMPAR-mediated excitatory postsynaptic currents at Schaffer collateral - CA1 pyramidal neuron synapses during ESE. Surface expression of the GluA1 subunit increased, and this was a consequence of N-methyl-d-aspartate receptor activation. Further, diminishing glutamate release by activation of somatostatin receptors prevented SE. These studies suggest that AMPAR-mediated glutamatergic transmission is strengthened during ESE.

摘要

癫痫持续状态(SE)与突触后神经递质受体的动态可塑性有关。在苯二氮䓬类药物耐药后建立的 SE(ESE)期间,评估了 AMPA 受体(AMPAR)-介导的谷氨酸能传递的可塑性。在 ESE 期间,Schaffer 侧枝-CA1 锥体神经元突触处 AMPAR 介导的兴奋性突触后电流的频率和内向整流增加。GluA1 亚基的表面表达增加,这是 N-甲基-D-天冬氨酸受体激活的结果。此外,通过激活生长抑素受体减少谷氨酸释放可防止 SE。这些研究表明,在 ESE 期间 AMPAR 介导的谷氨酸能传递增强。

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