NMDA receptor-mediated immediate Ser831 phosphorylation of GluR1 through CaMKIIα in rat hippocampus during early global ischemia

Xin Zhen Fu, Quanguang Zhang, Fan Jie Meng, Guang Yi Zhang

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

The phosphorylation of α-amino-3-hydroxy-5-methylisoxazole-4- propionic acid (AMPA) receptors subunit GluR1 at Ser831 has been implicated in the regulation of AMPA receptors channel. In this paper, Ser831 phosphorylation of GluR1 in rat hippocampus was investigated, which significantly increased during early global ischemia. To further illustrate the underlying mechanisms, calcium/calmodulin-dependent kinase IIα (CaMKIIα) inhibitor 1-[N,O-bis-(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine (KN62), CaM antagonist trifluoperazine (TFP), N-methyl-D-aspartate (NMDA) receptor antagonist dextromethorphan (DEX), AMPA receptor antagonist 6,7-dinitro-quinoxaline-2,3-(1H,4H)-dione (DNQX) and L-type voltage-gated Ca2+ channel (L-VGCC) blocker nifedipine (NIF), were respectively administrated to the rats 20min prior to ischemia. The results showed that KN62, TFP and DEX significantly attenuated Ser831 phosphorylation of GluR1, while DNQX and NIF had no obvious effects. Consequently, the studies suggest that early global ischemia induced Ser831 phosphorylation of GluR1 may be closely associated with CaMKIIα and the NMDA receptor, while the immediate Ser831 phosphorylation of GluR1 may have been involved in pathogenic events after early global ischemia.

Original languageEnglish (US)
Pages (from-to)85-91
Number of pages7
JournalNeuroscience Research
Volume48
Issue number1
DOIs
StatePublished - Jan 1 2004
Externally publishedYes

Fingerprint

Calcium-Calmodulin-Dependent Protein Kinases
N-Methyl-D-Aspartate Receptors
Hippocampus
Ischemia
Phosphorylation
Dextromethorphan
Trifluoperazine
KN 62
Nifedipine
Quinoxalines
Calcium
bucide
propionic acid

Keywords

  • Calcium/calmodulin-dependent kinase IIα
  • GluR1
  • Ischemia
  • N-Methyl-D-aspartate receptor
  • Phosphorylation
  • α-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

NMDA receptor-mediated immediate Ser831 phosphorylation of GluR1 through CaMKIIα in rat hippocampus during early global ischemia. / Fu, Xin Zhen; Zhang, Quanguang; Meng, Fan Jie; Zhang, Guang Yi.

In: Neuroscience Research, Vol. 48, No. 1, 01.01.2004, p. 85-91.

Research output: Contribution to journalArticle

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abstract = "The phosphorylation of α-amino-3-hydroxy-5-methylisoxazole-4- propionic acid (AMPA) receptors subunit GluR1 at Ser831 has been implicated in the regulation of AMPA receptors channel. In this paper, Ser831 phosphorylation of GluR1 in rat hippocampus was investigated, which significantly increased during early global ischemia. To further illustrate the underlying mechanisms, calcium/calmodulin-dependent kinase IIα (CaMKIIα) inhibitor 1-[N,O-bis-(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine (KN62), CaM antagonist trifluoperazine (TFP), N-methyl-D-aspartate (NMDA) receptor antagonist dextromethorphan (DEX), AMPA receptor antagonist 6,7-dinitro-quinoxaline-2,3-(1H,4H)-dione (DNQX) and L-type voltage-gated Ca2+ channel (L-VGCC) blocker nifedipine (NIF), were respectively administrated to the rats 20min prior to ischemia. The results showed that KN62, TFP and DEX significantly attenuated Ser831 phosphorylation of GluR1, while DNQX and NIF had no obvious effects. Consequently, the studies suggest that early global ischemia induced Ser831 phosphorylation of GluR1 may be closely associated with CaMKIIα and the NMDA receptor, while the immediate Ser831 phosphorylation of GluR1 may have been involved in pathogenic events after early global ischemia.",
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AB - The phosphorylation of α-amino-3-hydroxy-5-methylisoxazole-4- propionic acid (AMPA) receptors subunit GluR1 at Ser831 has been implicated in the regulation of AMPA receptors channel. In this paper, Ser831 phosphorylation of GluR1 in rat hippocampus was investigated, which significantly increased during early global ischemia. To further illustrate the underlying mechanisms, calcium/calmodulin-dependent kinase IIα (CaMKIIα) inhibitor 1-[N,O-bis-(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperazine (KN62), CaM antagonist trifluoperazine (TFP), N-methyl-D-aspartate (NMDA) receptor antagonist dextromethorphan (DEX), AMPA receptor antagonist 6,7-dinitro-quinoxaline-2,3-(1H,4H)-dione (DNQX) and L-type voltage-gated Ca2+ channel (L-VGCC) blocker nifedipine (NIF), were respectively administrated to the rats 20min prior to ischemia. The results showed that KN62, TFP and DEX significantly attenuated Ser831 phosphorylation of GluR1, while DNQX and NIF had no obvious effects. Consequently, the studies suggest that early global ischemia induced Ser831 phosphorylation of GluR1 may be closely associated with CaMKIIα and the NMDA receptor, while the immediate Ser831 phosphorylation of GluR1 may have been involved in pathogenic events after early global ischemia.

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