Hurtado-Zavala, Joaqúin Isaac

[["dc.bibliographiccitation.artnumber","15878"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Hurtado-Zavala, Joaquin I."],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Halder, Rashi"],["dc.contributor.author","Bolleyer, Christiane"],["dc.contributor.author","Awasthi, Ankit"],["dc.contributor.author","Stahlberg, Markus A."],["dc.contributor.author","Wagener, Robin J."],["dc.contributor.author","Anderson, Kristin"],["dc.contributor.author","Drenan, Ryan M."],["dc.contributor.author","Lester, Henry A."],["dc.contributor.author","Miwa, Julie M."],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2018-04-23T11:47:16Z"],["dc.date.available","2018-04-23T11:47:16Z"],["dc.date.issued","2017"],["dc.description.abstract","TRPV1 is an ion channel activated by heat and pungent agents including capsaicin, and has been extensively studied in nociception of sensory neurons. However, the location and function of TRPV1 in the hippocampus is debated. We found that TRPV1 is expressed in oriens-lacunosum-moleculare (OLM) interneurons in the hippocampus, and promotes excitatory innervation. TRPV1 knockout mice have reduced glutamatergic innervation of OLM neurons. When activated by capsaicin, TRPV1 recruits more glutamatergic, but not GABAergic, terminals to OLM neurons in vitro. When TRPV1 is blocked, glutamatergic input to OLM neurons is dramatically reduced. Heterologous expression of TRPV1 also increases excitatory innervation. Moreover, TRPV1 knockouts have reduced Schaffer collateral LTP, which is rescued by activating OLM neurons with nicotine—via α2β2-containing nicotinic receptors—to bypass innervation defects. Our results reveal a synaptogenic function of TRPV1 in a specific interneuron population in the hippocampus, where it is important for gating hippocampal plasticity."],["dc.identifier.doi","10.1038/ncomms15878"],["dc.identifier.gro","3142196"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14910"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13316"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.issn","2041-1723"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","TRPV1 regulates excitatory innervation of OLM neurons in the hippocampus"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1087"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cerebral Cortex"],["dc.bibliographiccitation.lastpage","1104"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Hurtado-Zavala, Joaquin I"],["dc.contributor.author","Awasthi, Ankit"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Faram, Ruth"],["dc.contributor.author","Ahmad, Hamid"],["dc.contributor.author","Swaminathan, Aarti"],["dc.contributor.author","McIlhinney, Jeffrey"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Perestenko, Pavel"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2018-01-09T14:34:30Z"],["dc.date.available","2018-01-09T14:34:30Z"],["dc.date.issued","2017"],["dc.description.abstract","Dendritic spines compartmentalize information in the brain, and their morphological characteristics are thought to underly synaptic plasticity. Here we identify copine-6 as a novel modulator of dendritic spine morphology. We found that brain-derived neurotrophic factor (BDNF) - a molecule essential for long-term potentiation of synaptic strength - upregulated and recruited copine-6 to dendritic spines in hippocampal neurons. Overexpression of copine-6 increased mushroom spine number and decreased filopodia number, while copine-6 knockdown had the opposite effect and dramatically increased the number of filopodia, which lacked PSD95. Functionally, manipulation of post-synaptic copine-6 levels affected miniature excitatory post-synaptic current (mEPSC) kinetics and evoked synaptic vesicle recycling in contacting boutons, and post-synaptic knockdown of copine-6 reduced hippocampal LTP and increased LTD. Mechanistically, copine-6 promotes BDNF-TrkB signaling and recycling of activated TrkB receptors back to the plasma membrane surface, and is necessary for BDNF-induced increases in mushroom spines in hippocampal neurons. Thus copine-6 regulates BDNF-dependent changes in dendritic spine morphology to promote synaptic plasticity."],["dc.identifier.doi","10.1093/cercor/bhx009"],["dc.identifier.pmid","28158493"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11602"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1460-2199"],["dc.title","Regulation of Dendritic Spine Morphology in Hippocampal Neurons by Copine-6"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]