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  Priming of long-term potentiation in mouse hippocampus by corticotropin-releasing factor and acute stress: Implications for hippocampus-dependent learning

Blank, T., Nijholt, I., Eckart, K., & Spiess, J. (2002). Priming of long-term potentiation in mouse hippocampus by corticotropin-releasing factor and acute stress: Implications for hippocampus-dependent learning. The Journal of Neuroscience: the Official Journal of the Society for Neuroscience, 22(9), 3788-3794.

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 Creators:
Blank, Thomas1, Author           
Nijholt, Ingrid1, Author           
Eckart, Klaus1, Author           
Spiess, Joachim1, Author           
Affiliations:
1Molecular neuroendocrinology, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173662              

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Free keywords: priming; neuronal excitability; h/rCRF; CaMKII; LTP; PKC; classical fear conditioning
 Abstract: In the present experiments, we characterized the action of human/rat corticotropin-releasing factor (h/rCRF) and acute stress (1 hr of immobilization) on hippocampus-dependent learning and on synaptic plasticity in the mouse hippocampus. We first showed that h/rCRF application and acute stress facilitated (primed) long-term potentiation of population spikes (PS-LTP) in the mouse hippocampus and enhanced context- dependent fear conditioning. Both the priming of PS-LTP and the improvement of context-dependent fear conditioning were prevented by the CRF receptor antagonist [Glu(11,16)]astressin. PS-LTP priming and improved learning were also reduced by the protein kinase C inhibitor bisindolylmaleimide I. Acute stress induced the activation of Ca2+/calmodulin-dependent kinase II (CaMKII) 2 hr after the end of the stress session. The CaMKII inhibitor KN-62 antagonized the stress-mediated learning enhancement, however, with no effect on PS-LTP persistence. Thus, long-lasting increased neuronal excitability as reflected in PS-LTP priming appeared to be essential for the enhancement of learning in view of the observation that inhibition of PS- LTP priming was associated with impaired learning. Conversely, it was demonstrated that inhibition of CaMKII activity reduced contextual fear conditioning without affecting PS-LTP priming. This observation suggests that priming of PS-LTP and activation of CaMKII represent two essential mechanisms that may contribute independently to long-term memory.

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Language(s): eng - English
 Dates: 2002-05-01
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 18997
ISI: 000175296200055
 Degree: -

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Title: The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
  Other : J. Neurosci.
Source Genre: Journal
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Affiliations:
Publ. Info: Baltimore, MD : The Society
Pages: - Volume / Issue: 22 (9) Sequence Number: - Start / End Page: 3788 - 3794 Identifier: ISSN: 0270-6474
CoNE: https://pure.mpg.de/cone/journals/resource/954925502187_1