Enhanced phosphorylation of the postsynaptic protein kinase C substrate RC3/neurogranin during long-term potentiation

Shu Jen Chen, J. David Sweatt, Eric Klann

Research output: Contribution to journalArticle

Abstract

Long-term potentiation (LTP) is a sustained strengthening of synaptic connections that occurs in the mammalian hippocampus, and is a cellular mechanism likely to contribute to memory formation. One question of current interest is whether the biochemical mechanisms responsible for the maintenance of LTP have a presynaptic or postsynaptic locus. We have determined that the phosphorylation of the postsynaptic protein kinase (PKC) substrate RC3/neurogranin is increased in the maintenance phase of LTP, and that the induction of this effect is dependent on activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors. The sustained increase in RC3/neurogranin phosphorylation requires ongoing protein kinase activity, as application of the protein kinase inhibitor H-7 after LTP induction can reverse the increased RC3/neurogranin phosphorylation. Overall, these data are evidence for postsynaptic biochemical changes in the maintenance of LTP. They also implicate RC3/neurogranin as a downstream effector of PKC activity in LTP that could contribute to physiologic expression of LTP.

Original languageEnglish (US)
Pages (from-to)181-187
Number of pages7
JournalBrain Research
Volume749
Issue number2
DOIs
StatePublished - Feb 28 1997

Fingerprint

Neurogranin
Long-Term Potentiation
Protein Kinase C
Phosphorylation
Maintenance
Protein Kinases
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
Glutamate Receptors
N-Methylaspartate
Protein Kinase Inhibitors
Hippocampus

Keywords

  • calmodulin
  • hippocampus
  • learning and memory
  • postsynaptic protein
  • protein kinase C substrate
  • synaptic plasticity

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Enhanced phosphorylation of the postsynaptic protein kinase C substrate RC3/neurogranin during long-term potentiation. / Chen, Shu Jen; Sweatt, J. David; Klann, Eric.

In: Brain Research, Vol. 749, No. 2, 28.02.1997, p. 181-187.

Research output: Contribution to journalArticle

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N2 - Long-term potentiation (LTP) is a sustained strengthening of synaptic connections that occurs in the mammalian hippocampus, and is a cellular mechanism likely to contribute to memory formation. One question of current interest is whether the biochemical mechanisms responsible for the maintenance of LTP have a presynaptic or postsynaptic locus. We have determined that the phosphorylation of the postsynaptic protein kinase (PKC) substrate RC3/neurogranin is increased in the maintenance phase of LTP, and that the induction of this effect is dependent on activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors. The sustained increase in RC3/neurogranin phosphorylation requires ongoing protein kinase activity, as application of the protein kinase inhibitor H-7 after LTP induction can reverse the increased RC3/neurogranin phosphorylation. Overall, these data are evidence for postsynaptic biochemical changes in the maintenance of LTP. They also implicate RC3/neurogranin as a downstream effector of PKC activity in LTP that could contribute to physiologic expression of LTP.

AB - Long-term potentiation (LTP) is a sustained strengthening of synaptic connections that occurs in the mammalian hippocampus, and is a cellular mechanism likely to contribute to memory formation. One question of current interest is whether the biochemical mechanisms responsible for the maintenance of LTP have a presynaptic or postsynaptic locus. We have determined that the phosphorylation of the postsynaptic protein kinase (PKC) substrate RC3/neurogranin is increased in the maintenance phase of LTP, and that the induction of this effect is dependent on activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors. The sustained increase in RC3/neurogranin phosphorylation requires ongoing protein kinase activity, as application of the protein kinase inhibitor H-7 after LTP induction can reverse the increased RC3/neurogranin phosphorylation. Overall, these data are evidence for postsynaptic biochemical changes in the maintenance of LTP. They also implicate RC3/neurogranin as a downstream effector of PKC activity in LTP that could contribute to physiologic expression of LTP.

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