Ramachandran, Binu

[["dc.bibliographiccitation.artnumber","27"],["dc.bibliographiccitation.journal","Frontiers in synaptic neuroscience"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Shinoda, Yo"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Bharat, Vinita"],["dc.contributor.author","Brockelt, David"],["dc.contributor.author","Altas, Bekir"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2019-07-09T11:41:08Z"],["dc.date.available","2019-07-09T11:41:08Z"],["dc.date.issued","2014"],["dc.description.abstract","Brain-derived neurotrophic factor (BDNF) is widely reported to enhance synaptic vesicle (SV) exocytosis and neurotransmitter release. But it is still unclear whether BDNF enhances SV recycling at excitatory terminals only, or at both excitatory and inhibitory terminals. In the present study, in a direct comparison using cultured rat hippocampal neurons, we demonstrate that BDNF enhances both spontaneous and activity-dependent neurotransmitter release from excitatory terminals, but not from inhibitory terminals. BDNF treatment for 5 min or 48 h increased both spontaneous and activity-induced anti-synaptotagmin1 (SYT1) antibody uptake at excitatory terminals marked with vGluT1. Conversely, BDNF treatment did not enhance spontaneous or activity-induced uptake of anti-SYT1 antibodies in inhibitory terminals marked with vGAT. Time-lapse imaging of FM1-43 dye destaining in excitatory and inhibitory terminals visualized by post-hoc immunostaining of vGluT1 and vGAT also showed the same result: The rate of spontaneous and activity-induced destaining was increased by BDNF at excitatory synapses, but not at inhibitory synapses. These data demonstrate that BDNF enhances SV exocytosis in excitatory but not inhibitory terminals. Moreover, BDNF enhanced evoked SV exocytosis, even if vesicles were loaded under spontaneous vesicle recycling conditions. Thus, BDNF enhances both spontaneous and activity-dependent neurotransmitter release on both short and long time-scales, by the same mechanism."],["dc.identifier.doi","10.3389/fnsyn.2014.00027"],["dc.identifier.fs","607146"],["dc.identifier.pmid","25426063"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11694"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58356"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/260916/EU//SYT"],["dc.relation.euproject","SytActivity"],["dc.relation.issn","1663-3563"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","BDNF enhances spontaneous and activity-dependent neurotransmitter release at excitatory terminals but not at inhibitory terminals in hippocampal neurons."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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.artnumber","23"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Frontiers in Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","10"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2019-07-09T11:41:03Z"],["dc.date.available","2019-07-09T11:41:03Z"],["dc.date.issued","2015"],["dc.description.abstract","Information storage in CA1 hippocampal pyramidal neurons is compartmentalized in proximal vs. distal apical dendrites, cell bodies, and basal dendrites. This compartmentalization is thought to be essential for synaptic integration. Differences in the expression of long-term potentiation (LTP) in each of these compartments have been described, but less is known regarding potential differences in long-term depression (LTD). Here, to directly compare LTD expression in each compartment and to bypass possible differences in input-specificity and stimulation of presynaptic inputs, we used global application of NMDA to induce LTD. We then examined LTD expression in each dendritic sub-region—proximal and distal apical, and basal dendrites—and in cell bodies. Interestingly, we found that distal apical dendrites exhibited the greatest magnitude of LTD of all areas tested and this LTD was maintained, whereas LTD in proximal apical dendrites was not maintained. In basal dendrites, LTD was also maintained, but the magnitude of LTD was less than in distal apical dendrites. Blockade of inhibition blocked LTD maintenance in both distal apical and basal dendrites. Population spikes recorded from the cell body layer correlated with apical dendrite field EPSP (fEPSP), where LTD was maintained in distal dendrites and decayed in proximal dendrites. On the other hand, LTD of basal dendrite fEPSPs was maintained but population spike responses were not. Thus E-S coupling was distinct in basal and apical dendrites. Our data demonstrate cell autonomous differential information processing in somas and dendritic sub-regions of CA1 pyramidal neurons in the hippocampus, where LTD expression is intrinsic to distinct dendritic regions, and does not depend on the nature of stimulation and input specificity."],["dc.identifier.doi","10.3389/fncel.2015.00023"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11660"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58351"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/260916/EU//SYT"],["dc.relation.euproject","SytActivity"],["dc.relation.issn","1662-5102"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Long-term depression is differentially expressed in distinct lamina of hippocampal CA1 dendrites"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e1239"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Translational psychiatry"],["dc.bibliographiccitation.lastpage","e1239"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Benito, E."],["dc.contributor.author","Ramachandran, B."],["dc.contributor.author","Schroeder, H."],["dc.contributor.author","Schmidt, G."],["dc.contributor.author","Urbanke, H."],["dc.contributor.author","Burkhardt, S."],["dc.contributor.author","Capece, V."],["dc.contributor.author","Dean, C."],["dc.contributor.author","Fischer, A."],["dc.date.accessioned","2019-07-09T11:44:50Z"],["dc.date.available","2019-07-09T11:44:50Z"],["dc.date.issued","2017-09-26"],["dc.description.abstract","Histone acetylation is essential for memory formation and its deregulation contributes to the pathogenesis of Alzheimer's disease. Thus, targeting histone acetylation is discussed as a novel approach to treat dementia. The histone acetylation landscape is shaped by chromatin writer and eraser proteins, while readers link chromatin state to cellular function. Chromatin readers emerged novel drug targets in cancer research but little is known about the manipulation of readers in the adult brain. Here we tested the effect of JQ1-a small-molecule inhibitor of the chromatin readers BRD2, BRD3, BRD4 and BRDT-on brain function and show that JQ1 is able to enhance cognitive performance and long-term potentiation in wild-type animals and in a mouse model for Alzheimer's disease. Systemic administration of JQ1 elicited a hippocampal gene expression program that is associated with ion channel activity, transcription and DNA repair. Our findings suggest that JQ1 could be used as a therapy against dementia and should be further tested in the context of learning and memory."],["dc.identifier.doi","10.1038/tp.2017.202"],["dc.identifier.pmid","28949335"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14924"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59110"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/H2020/648898/EU//DEPICODE"],["dc.relation.issn","2158-3188"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","612"],["dc.title","The BET/BRD inhibitor JQ1 improves brain plasticity in WT and APP mice."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]