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Article: A novel mechanism for the facilitation of theta-induced long-term potentiation by brain-derived neurotrophic factor

TitleA novel mechanism for the facilitation of theta-induced long-term potentiation by brain-derived neurotrophic factor
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2004
PublisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.org
Citation
Journal of Neuroscience, 2004, v. 24 n. 22, p. 5151-5161 How to Cite?
AbstractBrain-derived neurotrophic factor (BDNF) contributes to the induction of long-term potentiation (LTP) by theta-pattern stimulation, but the specific processes underlying this effect are not known. Experiments described here, using BDNF concentrations that have minor effects on baseline responses, show that the neurotrophin both reduces the threshold for LTP induction and elevates the ceiling on maximal potentiation. The enhanced LTP proved to be as stable and resistant to reversal as that recorded under control conditions. BDNF markedly increased the facilitation of burst responses that occurs within a theta train. This suggests that the neurotrophin acts on long-lasting events that (1) are set in motion by the first burst in a train and (2) regulate the amplitude of subsequent bursts. Whole-cell recordings established that BDNF causes a rapid reduction in the size of the long-lasting afterhyperpolarization (AHP) that follows individual theta bursts. Apamin, an antagonist of type 2 small-conductance Ca2+-activated potassium (SK2) channels, also reduced hippocampal AHPs and closely reproduced the effects of BDNF on theta-burst responses and LTP. The latter results were replicated with a newly introduced, highly selective inhibitor of SK2 channels. Immunoblot analyses indicated that BDNF increases SK2 serine phosphorylation in hippocampal slices. These findings point to the conclusion that BDNF-driven protein kinase cascades serve to depress the SK2 component, and possibly other constituents, of the AHP. It is likely that this mechanism, acting with other factors, promotes the formation and increases the magnitude of LTP.
Persistent Identifierhttp://hdl.handle.net/10722/91052
ISSN
2015 Impact Factor: 5.924
2015 SCImago Journal Rankings: 5.105
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKramár, EAen_HK
dc.contributor.authorLin, Ben_HK
dc.contributor.authorLin, C-Yen_HK
dc.contributor.authorArai, ACen_HK
dc.contributor.authorGall, CMen_HK
dc.contributor.authorLynch, Gen_HK
dc.date.accessioned2010-09-17T10:12:19Z-
dc.date.available2010-09-17T10:12:19Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal of Neuroscience, 2004, v. 24 n. 22, p. 5151-5161en_HK
dc.identifier.issn0270-6474en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91052-
dc.description.abstractBrain-derived neurotrophic factor (BDNF) contributes to the induction of long-term potentiation (LTP) by theta-pattern stimulation, but the specific processes underlying this effect are not known. Experiments described here, using BDNF concentrations that have minor effects on baseline responses, show that the neurotrophin both reduces the threshold for LTP induction and elevates the ceiling on maximal potentiation. The enhanced LTP proved to be as stable and resistant to reversal as that recorded under control conditions. BDNF markedly increased the facilitation of burst responses that occurs within a theta train. This suggests that the neurotrophin acts on long-lasting events that (1) are set in motion by the first burst in a train and (2) regulate the amplitude of subsequent bursts. Whole-cell recordings established that BDNF causes a rapid reduction in the size of the long-lasting afterhyperpolarization (AHP) that follows individual theta bursts. Apamin, an antagonist of type 2 small-conductance Ca2+-activated potassium (SK2) channels, also reduced hippocampal AHPs and closely reproduced the effects of BDNF on theta-burst responses and LTP. The latter results were replicated with a newly introduced, highly selective inhibitor of SK2 channels. Immunoblot analyses indicated that BDNF increases SK2 serine phosphorylation in hippocampal slices. These findings point to the conclusion that BDNF-driven protein kinase cascades serve to depress the SK2 component, and possibly other constituents, of the AHP. It is likely that this mechanism, acting with other factors, promotes the formation and increases the magnitude of LTP.en_HK
dc.languageengen_HK
dc.publisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.orgen_HK
dc.relation.ispartofJournal of Neuroscienceen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titleA novel mechanism for the facilitation of theta-induced long-term potentiation by brain-derived neurotrophic factoren_HK
dc.typeArticleen_HK
dc.identifier.emailLin, B:blin@hku.hken_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1523/JNEUROSCI.0800-04.2004en_HK
dc.identifier.pmid15175384-
dc.identifier.scopuseid_2-s2.0-2642546665en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2642546665&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume24en_HK
dc.identifier.issue22en_HK
dc.identifier.spage5151en_HK
dc.identifier.epage5161en_HK
dc.identifier.isiWOS:000221883100008-

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