Status epilepticus impairs synaptic plasticity in rat hippocampus and is followed by changes in expression of NMDA receptors
- 作者: Postnikova T.1,2, Zubareva O.1,3, Kovalenko A.3, Kim K.1, Magazanik L.1,4, Zaitsev A.1
-
隶属关系:
- Sechenov Institute of Evolutionary Physiology and Biochemistry
- Peter the Great St. Petersburg Polytechnic University
- Institute of Experimental Medicine
- Saint Petersburg State University
- 期: 卷 82, 编号 3 (2017)
- 页面: 282-290
- 栏目: Article
- URL: https://journals.rcsi.science/0006-2979/article/view/151283
- DOI: https://doi.org/10.1134/S0006297917030063
- ID: 151283
如何引用文章
详细
Cognitive deficits and memory loss are frequent in patients with temporal lobe epilepsy. Persistent changes in synaptic efficacy are considered as a cellular substrate underlying memory processes. Electrophysiological studies have shown that the properties of short-term and long-term synaptic plasticity in the cortex and hippocampus may undergo substantial changes after seizures. However, the neural mechanisms responsible for these changes are not clear. In this study, we investigated the properties of short-term and long-term synaptic plasticity in rat hippocampal slices 24 h after pentylenetetrazole (PTZ)-induced status epilepticus. We found that the induction of long-term potentiation (LTP) in CA1 pyramidal cells is reduced compared to the control, while short-term facilitation is increased. The experimental results do not support the hypothesis that status epilepticus leads to background potentiation of hippocampal synapses and further LTP induction becomes weaker due to occlusion, as the dependence of synaptic responses on the strength of input stimulation was not different in the control and experimental animals. The decrease in LTP can be caused by impairment of molecular mechanisms of neuronal plasticity, including those associated with NMDA receptors and/or changes in their subunit composition. Realtime PCR demonstrated significant increases in the expression of GluN1 and GluN2A subunits 3 h after PTZ-induced status epilepticus. The overexpression of obligate GluN1 subunit suggests an increase in the total number of NMDA receptors in the hippocampus. A 3-fold increase in the expression of the GluN2B subunit observed 24 h after PTZ-induced status epilepticus might be indicative of an increase in the proportion of GluN2B-containing NMDA receptors. Increased expression of the GluN2B subunit may be a cause for reducing the magnitude of LTP at hippocampal synapses after status epilepticus.
作者简介
T. Postnikova
Sechenov Institute of Evolutionary Physiology and Biochemistry; Peter the Great St. Petersburg Polytechnic University
Email: aleksey_zaitsev@mail.ru
俄罗斯联邦, St. Petersburg, 194223; St. Petersburg, 195251
O. Zubareva
Sechenov Institute of Evolutionary Physiology and Biochemistry; Institute of Experimental Medicine
Email: aleksey_zaitsev@mail.ru
俄罗斯联邦, St. Petersburg, 194223; St. Petersburg, 197376
A. Kovalenko
Institute of Experimental Medicine
Email: aleksey_zaitsev@mail.ru
俄罗斯联邦, St. Petersburg, 197376
K. Kim
Sechenov Institute of Evolutionary Physiology and Biochemistry
Email: aleksey_zaitsev@mail.ru
俄罗斯联邦, St. Petersburg, 194223
L. Magazanik
Sechenov Institute of Evolutionary Physiology and Biochemistry; Saint Petersburg State University
Email: aleksey_zaitsev@mail.ru
俄罗斯联邦, St. Petersburg, 194223; St. Petersburg, 199034
A. Zaitsev
Sechenov Institute of Evolutionary Physiology and Biochemistry
编辑信件的主要联系方式.
Email: aleksey_zaitsev@mail.ru
俄罗斯联邦, St. Petersburg, 194223
![](/img/style/loading.gif)