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PKMζ Knockdown Disrupts Post-Ischemic Long-Term Potentiation via Inhibiting Postsynaptic Expression of Aminomethyl Phosphonic Acid Receptors

PKMζ Knockdown Disrupts Post-Ischemic Long-Term Potentiation via Inhibiting Postsynaptic Expression of Aminomethyl Phosphonic Acid Receptors

Nan Cheng, Xiaoqiao Hu, Tian Tian, Wei Lu

J Biomed Res. 2015 May;29(3):241-9.

PMID: 26060448

Abstract:

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 Mζ (PKMζ), an atypical protein kinase C isoform, was involved in enhancing aminomethyl phosphonic acid (AMPA) receptor (AMPAR) expression after i-LTP induction. PKMζ knockdown attenuated postsynaptic expression of AMPA receptors and disrupted i-LTP. Consistently, we observed less neuronal death of cultured hippocampal cells with PKMζ knockdown. Meanwhile, these findings indicate that PKMζ 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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP1066519-B	(Aminomethyl)phosphonic acid		1066-51-9	Price

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