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Article: Dual actions of brain-derived neurotrophic factor on GABAergic transmission in cerebellar Purkinje neurons

TitleDual actions of brain-derived neurotrophic factor on GABAergic transmission in cerebellar Purkinje neurons
Authors
Issue Date2012
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexnr
Citation
Experimental Neurology, 2012, v. 233 n. 2, p. 791-798 How to Cite?
AbstractThe ability to regulate inhibitory synapses is a critical feature of the nervous system and a growing body of evidence indicates that brain-derived neurotrophic factor (BDNF) acutely modulates the efficacy of GABA synaptic transmission. Although the neuronal potassium-chloride cotransporter 2 (KCC2) has been implied in this BDNF-induced ionic plasticity, the reports about actions of BDNF on GABA signaling remain conflicting. Here we show dual effects of BDNF on GABAergic synaptic transmission in Purkinje neurons in rat cerebellar slices. BDNF decreased the amplitude of evoked outward IPSCs postsynaptically. It induced a depolarizing shift in the reversal potential (E IPSC), which reduced the driving force for outward IPSCs. However, in the absence of KCC2 activity, BDNF directly potentiated rather than inhibited GABA A receptor, which was reflected by an increase in the amplitude of outward IPSCs. This action of BDNF coincided with its effect in increasing the amplitude of inward IPSCs. Furthermore, an interaction between GABA A receptor and KCC2 was revealed by co-immunoprecipitation. The effects of BDNF on both GABA A receptor and KCC2 were dependent on TrkB and also activation of cyclin-dependent kinase 5 (Cdk5). However, only the effect of BDNF on KCC2 activity was dependent on a rise of intracellular calcium. Taken together, these data highlight distinct actions of BDNF on KCC2 and GABA A receptor in the regulation of GABAergic synaptic transmission. © 2011 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/145822
ISSN
2015 Impact Factor: 4.657
2015 SCImago Journal Rankings: 2.427
ISI Accession Number ID
Funding AgencyGrant Number
Research Grants Council of Hong Kong2900336
NSFC/RGC from National Natural Science Foundation of China30931160433
Funding Information:

We thank Mr. Kenny Ho and Mr. Alan S.L. Wong for expert technical assistance. This work was supported by the Research Grants Council of Hong Kong (2900336) and the NSFC/RGC Joint Research Scheme 30931160433 from the National Natural Science Foundation of China.

References

 

DC FieldValueLanguage
dc.contributor.authorHuang, Yen_HK
dc.contributor.authorKo, Hen_HK
dc.contributor.authorCheung, ZHen_HK
dc.contributor.authorYung, KKLen_HK
dc.contributor.authorYao, Ten_HK
dc.contributor.authorWang, JJen_HK
dc.contributor.authorMorozov, Aen_HK
dc.contributor.authorKe, Yen_HK
dc.contributor.authorIp, NYen_HK
dc.contributor.authorYung, WHen_HK
dc.date.accessioned2012-03-23T09:49:50Z-
dc.date.available2012-03-23T09:49:50Z-
dc.date.issued2012en_HK
dc.identifier.citationExperimental Neurology, 2012, v. 233 n. 2, p. 791-798en_HK
dc.identifier.issn0014-4886en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145822-
dc.description.abstractThe ability to regulate inhibitory synapses is a critical feature of the nervous system and a growing body of evidence indicates that brain-derived neurotrophic factor (BDNF) acutely modulates the efficacy of GABA synaptic transmission. Although the neuronal potassium-chloride cotransporter 2 (KCC2) has been implied in this BDNF-induced ionic plasticity, the reports about actions of BDNF on GABA signaling remain conflicting. Here we show dual effects of BDNF on GABAergic synaptic transmission in Purkinje neurons in rat cerebellar slices. BDNF decreased the amplitude of evoked outward IPSCs postsynaptically. It induced a depolarizing shift in the reversal potential (E IPSC), which reduced the driving force for outward IPSCs. However, in the absence of KCC2 activity, BDNF directly potentiated rather than inhibited GABA A receptor, which was reflected by an increase in the amplitude of outward IPSCs. This action of BDNF coincided with its effect in increasing the amplitude of inward IPSCs. Furthermore, an interaction between GABA A receptor and KCC2 was revealed by co-immunoprecipitation. The effects of BDNF on both GABA A receptor and KCC2 were dependent on TrkB and also activation of cyclin-dependent kinase 5 (Cdk5). However, only the effect of BDNF on KCC2 activity was dependent on a rise of intracellular calcium. Taken together, these data highlight distinct actions of BDNF on KCC2 and GABA A receptor in the regulation of GABAergic synaptic transmission. © 2011 Elsevier Inc.en_HK
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexnren_HK
dc.relation.ispartofExperimental Neurologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnimals, Newbornen_HK
dc.subject.meshBrain-Derived Neurotrophic Factor - physiologyen_HK
dc.subject.meshCerebellum - metabolism - physiologyen_HK
dc.subject.meshInhibitory Postsynaptic Potentials - physiologyen_HK
dc.subject.meshOrgan Culture Techniquesen_HK
dc.subject.meshPurkinje Cells - metabolism - physiologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshReceptors, GABA-A - metabolismen_HK
dc.subject.meshSymporters - metabolismen_HK
dc.subject.meshSynaptic Transmission - physiologyen_HK
dc.subject.meshgamma-Aminobutyric Acid - physiologyen_HK
dc.titleDual actions of brain-derived neurotrophic factor on GABAergic transmission in cerebellar Purkinje neuronsen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, ZH:zelda@hku.hken_HK
dc.identifier.authorityCheung, ZH=rp01588en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.expneurol.2011.11.043en_HK
dc.identifier.pmid22178325-
dc.identifier.scopuseid_2-s2.0-84856550555en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84856550555&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume233en_HK
dc.identifier.issue2en_HK
dc.identifier.spage791en_HK
dc.identifier.epage798en_HK
dc.identifier.eissn1090-2430-
dc.identifier.isiWOS:000300123600027-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHuang, Y=47761147000en_HK
dc.identifier.scopusauthoridKo, H=54879810200en_HK
dc.identifier.scopusauthoridCheung, ZH=6507483375en_HK
dc.identifier.scopusauthoridYung, KKL=39763381500en_HK
dc.identifier.scopusauthoridYao, T=54879695000en_HK
dc.identifier.scopusauthoridWang, JJ=34772221200en_HK
dc.identifier.scopusauthoridMorozov, A=35110553600en_HK
dc.identifier.scopusauthoridKe, Y=7102816469en_HK
dc.identifier.scopusauthoridIp, NY=35318021000en_HK
dc.identifier.scopusauthoridYung, WH=7103137893en_HK
dc.identifier.citeulike10120746-

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