• ISSN 1674-8301
  • CN 32-1810/R
Volume 29 Issue 3
May  2015
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Nan Cheng, Xiaoqiao Hu, Tian Tian, Wei Lu. PKMf knockdown disrupts post-ischemic long-term potentiation via inhibiting postsynaptic expression of aminomethyl phosphonic acid receptors[J]. The Journal of Biomedical Research, 2015, 29(3): 241-249. doi: 10.7555/JBR.28.20140033
Citation: Nan Cheng, Xiaoqiao Hu, Tian Tian, Wei Lu. PKMf knockdown disrupts post-ischemic long-term potentiation via inhibiting postsynaptic expression of aminomethyl phosphonic acid receptors[J]. The Journal of Biomedical Research, 2015, 29(3): 241-249. doi: 10.7555/JBR.28.20140033

PKMf knockdown disrupts post-ischemic long-term potentiation via inhibiting postsynaptic expression of aminomethyl phosphonic acid receptors

doi: 10.7555/JBR.28.20140033
  • Received: 2014-02-25
  • Revised: 2014-03-11
  • Issue Date: 2015-05-29
  • Post-ischemic long-term potentiation (i-LTP) is a pathological form of plasticity that was observed in glutamate receptor-mediated neurotransmission after stroke and may exert a detrimental effect via facilitating excitotoxic damage. The mechanism underlying i-LTP, however, remains less understood. By employing electrophysiological recording and immunofluorescence assay on hippocampal slices and cultured neurons, we found that protein kinase Mf (PKMf), an atypical protein kinase C isoform, was involved in enhancing aminomethyl phosphonic acid (AMPA) receptor (AMPAR) expression after i-LTP induction. PKMf knockdown attenuated postsynaptic expression of AMPA receptors and disrupted i-LTP. Consistently, we observed less neuronal death of cultured hippocampal cells with PKMf knockdown. Meanwhile, these findings indicate that PKMf plays an important role in i-LTP by regulating postsynaptic expression of AMPA receptors. This work adds new knowledge to the mechanism of i-LTP,and thus is helpful to find the potential target for clinical therapy of ischemic stroke.

     

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