Hippocampal ischemia causes deficits in local field potential and synaptic plasticity |
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Authors: | Shaoli Wang Jingyun Zhang Tao Sheng Wei Lu Dengshun Miao |
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Institution: | 1The Research Center for Bone and Stem Cells, Department of Human Anatomy;2Department of Neurobiology;3The Center of Metabolic Disease Research, Nanjing Medical University, Nanjing, Jiangsu 210029, China;4The Key Laboratory of Developmental Genes and Human Disease, Institute of Life Sciences, Southeast University, Nanjing, Jiangsu 210096, China |
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Abstract: | 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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Keywords: | long-term potentiation local field potential ischemia endothelin-1 multi-channel in vivo recording |
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