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CaMKII requirement for the persistence of in vivo hippocampal mossy fiber synaptic plasticity and structural reorganization.

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Affiliations

  • 1. División de Investigación y Estudios de Posgrado, Facultad de Psicología, Universidad Nacional Autónoma de México, 04510 México, Mexico.
      Authors
    • Juárez-Muñoz Y 1
    • Rivera-Olvera A 1
    • Ramos-Languren LE 1
    • Escobar ML 1
    (4 authors)

ORCIDs linked to this article

Neurobiology of Learning and Memory, 27 Dec 2016, 139:56-62
https://doi.org/10.1016/j.nlm.2016.12.015 PMID: 28039086 

Abstract 

CaMKII has been proposed as a molecular substrate for long-term memory storage due to its capacity to maintain an active autophosporylated state even after the decay of the external stimuli. The hippocampal mossy fiber-CA3 pathway (MF-CA3) is considered as a relevant area for acquisition and storage of different learning tasks. MF-CA3 pathway exhibits a form of LTP characterized by a slow initial increase in the EPSP slope that is independent of NMDA receptors activation. Our previous studies show that application of high frequency stimulation sufficient to elicit MF-CA3 LTP produces structural reorganization, in a manner independent of LTP induction, at the stratum oriens of hippocampal CA3 area 7days after stimulation. However, the molecular mechanisms that underlie the maintenance of MF-CA3 LTP as well as the concomitant structural reorganization in this area remain to be elucidated. Here we show that acute microinfusion of myr-CaMKIINtide, a noncompetitive inhibitor of CaMKII, in the hippocampal CA3 area of adult rats during the late-phase of in vivo MF-CA3 LTP blocked its maintenance and prevented the accompanying morphological reorganization in CA3 area. These findings support the idea that CaMKII is a key molecular substrate for the long-term hippocampal synaptic plasticity maintenance.

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Read article at publisher's site: https://doi.org/10.1016/j.nlm.2016.12.015

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