4.6

CiteScore

2.2

Impact Factor
  • ISSN 1674-8301
  • CN 32-1810/R
Shaoli Wang, Jingyun Zhang, Tao Sheng, Wei Lu, Dengshun Miao. Hippocampal ischemia causes deficits in local field potential and synaptic plasticity[J]. The Journal of Biomedical Research, 2015, 29(5): 370-379. DOI: 10.7555/JBR.29.20150010
Citation: Shaoli Wang, Jingyun Zhang, Tao Sheng, Wei Lu, Dengshun Miao. Hippocampal ischemia causes deficits in local field potential and synaptic plasticity[J]. The Journal of Biomedical Research, 2015, 29(5): 370-379. DOI: 10.7555/JBR.29.20150010

Hippocampal ischemia causes deficits in local field potential and synaptic plasticity

Funds: 

Major State Basic Research ProgramofChina (Grant No. 2013CB733801)

More Information
  • Received Date: January 12, 2015
  • Revised Date: March 15, 2015
  • The long-term enhancement in glutamate receptor mediated excitatory responses has been observed in stroke model. This pathological form of plasticity, termed post-ischemic long-term potentiation (i-LTP), points to functional reorganization after stroke. Little is known, however, about whether and how this i-LTP would affect subsequent induction of synaptic plasticity. Here, we first directly confirmed that i-LTP was induced in the endothelin-1-induced ischemia model as in other in vitro models. We also demonstrated increased expression of NR2B, CaMKII and p-CaMKII, which are reminiscent of i-LTP. We further induced LTP of field excitatory postsynaptic potentials (fEPSPs) on CA1 hippocampal neurons in peri-infarct regions of the endothelin-1-induced mini-stroke model. We found that LTP of fEPSPs, induced by high-frequency stimulation, displayed a progressive impairment at 12 and 24 hours after ischemia. Moreover, using in vivo multi-channel recording, we found that the local field potential, which represents electrical property of cell ensembles in more restricted regions, was also dampened at these two time points. These results suggest that i-LTP elevates the induction threshold of subsequent synaptic plasticity. Our data helps to deepen the knowledge of meta-synaptic regulation of plasticity after focal ischemia.
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    2. Xiang Q, Li XH, Yang B, et al. Allicin attenuates tunicamycin-induced cognitive deficits in rats via its synaptic plasticity regulatory activity. Iran J Basic Med Sci, 2017, 20(6): 676-682. DOI:10.22038/IJBMS.2017.8837

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