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Article: Ketamine and selective activation of parvalbumin interneurons inhibit stress-induced dendritic spine elimination

TitleKetamine and selective activation of parvalbumin interneurons inhibit stress-induced dendritic spine elimination
Authors
Issue Date2018
PublisherNature Publishing Group: Open Access Journals - Option B. The Journal's web site is located at http://www.nature.com/tp/index.html
Citation
Translational Psychiatry, 2018, v. 8, article no. 272, p. 1-15 How to Cite?
AbstractStress is a major risk factor for the onset of many psychiatric diseases. In rodent models, chronic stress induces depression and impairs excitatory neurotransmission. However, little is known about the effect of stress on synaptic circuitry during the development of behavioral symptoms. Using two-photon transcranial imaging, we studied the effect of repeated restraint stress on dendritic spine plasticity in the frontal cortex in vivo. We found that restraint stress induced dendritic spine loss by decreasing the rate of spine formation and increasing the rate of spine elimination. The N-methyl-D-aspartate receptor antagonist ketamine inhibited stress-induced spine loss mainly by protecting mushroom spines from elimination. Ketamine also induced re-formation of spines in close proximity to previously stress-eliminated spines. Electrophysiological and in vivo imaging experiments showed that ketamine enhanced activity of parvalbumin (PV) interneurons under stress and counterbalanced the stress-induced net loss of PV axonal boutons. In addition, selective chemogenetic excitation of PV interneurons mimicked the protective effects of ketamine on dendritic spines against stress. Collectively, our data provide new insights on the effects of ketamine on synaptic circuitry under stress and a possible mechanism to counteract stress-induced synaptic impairments through PV interneuron activation.
Persistent Identifierhttp://hdl.handle.net/10722/268277
ISSN
2019 Impact Factor: 5.28
2015 SCImago Journal Rankings: 3.057
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorNg, HLL-
dc.contributor.authorHuang, Y-
dc.contributor.authorHan, L-
dc.contributor.authorChang, RCC-
dc.contributor.authorChan, YS-
dc.contributor.authorLai, SWC-
dc.date.accessioned2019-03-18T04:22:17Z-
dc.date.available2019-03-18T04:22:17Z-
dc.date.issued2018-
dc.identifier.citationTranslational Psychiatry, 2018, v. 8, article no. 272, p. 1-15-
dc.identifier.issn2158-3188-
dc.identifier.urihttp://hdl.handle.net/10722/268277-
dc.description.abstractStress is a major risk factor for the onset of many psychiatric diseases. In rodent models, chronic stress induces depression and impairs excitatory neurotransmission. However, little is known about the effect of stress on synaptic circuitry during the development of behavioral symptoms. Using two-photon transcranial imaging, we studied the effect of repeated restraint stress on dendritic spine plasticity in the frontal cortex in vivo. We found that restraint stress induced dendritic spine loss by decreasing the rate of spine formation and increasing the rate of spine elimination. The N-methyl-D-aspartate receptor antagonist ketamine inhibited stress-induced spine loss mainly by protecting mushroom spines from elimination. Ketamine also induced re-formation of spines in close proximity to previously stress-eliminated spines. Electrophysiological and in vivo imaging experiments showed that ketamine enhanced activity of parvalbumin (PV) interneurons under stress and counterbalanced the stress-induced net loss of PV axonal boutons. In addition, selective chemogenetic excitation of PV interneurons mimicked the protective effects of ketamine on dendritic spines against stress. Collectively, our data provide new insights on the effects of ketamine on synaptic circuitry under stress and a possible mechanism to counteract stress-induced synaptic impairments through PV interneuron activation.-
dc.languageeng-
dc.publisherNature Publishing Group: Open Access Journals - Option B. The Journal's web site is located at http://www.nature.com/tp/index.html-
dc.relation.ispartofTranslational Psychiatry-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleKetamine and selective activation of parvalbumin interneurons inhibit stress-induced dendritic spine elimination-
dc.typeArticle-
dc.identifier.emailHan, L: rahanlei@hku.hk-
dc.identifier.emailChang, RCC: rccchang@hku.hk-
dc.identifier.emailChan, YS: yschan@hku.hk-
dc.identifier.emailLai, SWC: coraswl@hku.hk-
dc.identifier.authorityChang, RCC=rp00470-
dc.identifier.authorityChan, YS=rp00318-
dc.identifier.authorityLai, SWC=rp01895-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41398-018-0321-5-
dc.identifier.pmid30531859-
dc.identifier.pmcidPMC6288154-
dc.identifier.scopuseid_2-s2.0-85058160256-
dc.identifier.hkuros297057-
dc.identifier.volume8-
dc.identifier.spagearticle no. 272, p. 1-
dc.identifier.epagearticle no. 272, p. 15-
dc.identifier.isiWOS:000452788700002-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl2158-3188-

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