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

Oh, M. Mathew, McKay, Bridget M., Power, John M. and Disterhoft, John F. (2009) Learning-related postburst afterhyperpolarization reduction in CA1 pyramidal neurons is mediated by protein kinase A. Proceedings of the National Academy of Science of the United States of America - PNAS, 106 5: 1620-1625. doi:10.1073/pnas.0807708106


Author Oh, M. Mathew
McKay, Bridget M.
Power, John M.
Disterhoft, John F.
Title Learning-related postburst afterhyperpolarization reduction in CA1 pyramidal neurons is mediated by protein kinase A
Journal name Proceedings of the National Academy of Science of the United States of America - PNAS   Check publisher's open access policy
ISSN 0027-8424
1091-6490
Publication date 2009-02-03
Year available 2009
Sub-type Article (original research)
DOI 10.1073/pnas.0807708106
Open Access Status Not Open Access
Volume 106
Issue 5
Start page 1620
End page 1625
Total pages 6
Editor Richard F. Thompson
Place of publication Washington, DC, United States
Publisher National Academy of Science
Language eng
Subject C1
110903 Central Nervous System
110902 Cellular Nervous System
920112 Neurodegenerative Disorders Related to Ageing
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.
Keyword Hippocampus
Protein kinase C
Trace eyeblink
Q-Index Code C1
Q-Index Status Confirmed Code

Document type: Journal Article
Sub-type: Article (original research)
Collections: 2010 Higher Education Research Data Collection
Queensland Brain Institute Publications
 
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Created: Sat, 09 May 2009, 02:23:47 EST by Debra McMurtrie on behalf of Queensland Brain Institute