BDNF Facilitates L-LTP Maintenance in the Absence of Protein Synthesis through PKMf

Hdl Handle:
http://hdl.handle.net/10675.2/662
Title:
BDNF Facilitates L-LTP Maintenance in the Absence of Protein Synthesis through PKMf
Authors:
Mei, Fan; Nagappan, Guhan; Ke, Yang; Sacktor, Todd C.; Lu, Bai
Abstract:
Late-phase long term potentiation (L-LTP) is thought to be the cellular basis for long-term memory (LTM). While LTM as well as L-LTP is known to depend on transcription and translation, it is unclear why brain-derived neurotrophic factor (BDNF) could sustain L-LTP when protein synthesis is inhibited. The persistently active protein kinase f (PKMf) is the only molecule implicated in perpetuating L-LTP maintenance. Here, in mouse acute brain slices, we show that inhibition of PKMf reversed BDNF-dependent form of L-LTP. While BDNF did not alter the steady-state level of PKMf, BDNF together with the L-LTP inducing theta-burst stimulation (TBS) increased PKMf level even without protein synthesis. Finally, in the absence of de novo protein synthesis, BDNF maintained TBS-induced PKMf at a sufficient level. These results suggest that BDNF sustains L-LTP through PKMf in a protein synthesis-independent manner, revealing an unexpected link between BDNF and PKMf.
Editors:
Mei, Lin
Citation:
PLoS One. 2011 Jun 29; 6(6):e21568
Issue Date:
29-Jun-2011
URI:
http://hdl.handle.net/10675.2/662
DOI:
10.1371/journal.pone.0021568
PubMed ID:
21747912
PubMed Central ID:
PMC3126837
Type:
Article
ISSN:
1932-6203
Appears in Collections:
Department of Neurology: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorMei, Fanen_US
dc.contributor.authorNagappan, Guhanen_US
dc.contributor.authorKe, Yangen_US
dc.contributor.authorSacktor, Todd C.en_US
dc.contributor.authorLu, Baien_US
dc.contributor.editorMei, Lin-
dc.date.accessioned2012-10-26T16:27:00Z-
dc.date.available2012-10-26T16:27:00Z-
dc.date.issued2011-06-29en_US
dc.identifier.citationPLoS One. 2011 Jun 29; 6(6):e21568en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid21747912en_US
dc.identifier.doi10.1371/journal.pone.0021568en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/662-
dc.description.abstractLate-phase long term potentiation (L-LTP) is thought to be the cellular basis for long-term memory (LTM). While LTM as well as L-LTP is known to depend on transcription and translation, it is unclear why brain-derived neurotrophic factor (BDNF) could sustain L-LTP when protein synthesis is inhibited. The persistently active protein kinase f (PKMf) is the only molecule implicated in perpetuating L-LTP maintenance. Here, in mouse acute brain slices, we show that inhibition of PKMf reversed BDNF-dependent form of L-LTP. While BDNF did not alter the steady-state level of PKMf, BDNF together with the L-LTP inducing theta-burst stimulation (TBS) increased PKMf level even without protein synthesis. Finally, in the absence of de novo protein synthesis, BDNF maintained TBS-induced PKMf at a sufficient level. These results suggest that BDNF sustains L-LTP through PKMf in a protein synthesis-independent manner, revealing an unexpected link between BDNF and PKMf.en_US
dc.rightsMei et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectNeuroscienceen_US
dc.subjectDevelopmental Neuroscienceen_US
dc.subjectSynaptic Plasticityen_US
dc.subjectMolecular Neuroscienceen_US
dc.subjectSignaling Pathwaysen_US
dc.subjectNeurophysiologyen_US
dc.subjectSynapsesen_US
dc.subjectLearning and Memoryen_US
dc.titleBDNF Facilitates L-LTP Maintenance in the Absence of Protein Synthesis through PKMfen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3126837en_US
dc.contributor.corporatenameDepartment of Neurology-

Related articles on PubMed

All Items in Scholarly Commons are protected by copyright, with all rights reserved, unless otherwise indicated.