Learning-related postburst afterhyperpolarization reduction in CA1 pyramidal neurons is mediated by protein kinase A

M. Matthew Oh, Bridget M. McKay, John M. Power, John F. Disterhoft

Research output: Contribution to journalArticlepeer-review

55 Scopus citations

Abstract

Learning-related reductions of the postburst afterhyperpolarization (AHP) in hippocampal pyramidal neurons have been shown ex vivo, after trace eyeblink conditioning. The AHP is also reduced by many neuromodulators, such as norepinephrine, via activation of protein kinases. Trace eyeblink conditioning, like other hippocampus-dependent tasks, relies on protein synthesis for consolidating the learned memory. Protein kinase A (PKA) has been shown to be a key contributor for protein synthesis via the cAMP-response element-binding pathway. Here, we have explored a potential involvement of PKA and protein kinase C (PKC) in maintaining the learning-related postburst AHP reduction observed in CA1 pyramidal neurons. Bath application of isoproterenol (1 μM), a β-adrenergic agonist that activates PKA, significantly reduced the AHP in CA1 neurons from control animals, but not from rats that learned. This occlusion suggests that PKA activity is involved in maintaining the AHP reduction measured ex vivo after successful learning. In contrast, bath application of the PKC activator, (-) indolactam V (0.2 μM), significantly reduced the AHP in CA1 neurons from both control and trained rats, indicating that PKC activity is not involved in maintaining the AHP reduction at this point after learning.

Original languageEnglish (US)
Pages (from-to)1620-1625
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume106
Issue number5
DOIs
StatePublished - Feb 3 2009

Keywords

  • Hippocampus
  • Protein kinase C
  • Trace eyeblink

ASJC Scopus subject areas

  • General

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