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.firstpage","106"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Hippocampus"],["dc.bibliographiccitation.lastpage","118"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Zafar, Noman"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2018-11-07T10:04:08Z"],["dc.date.available","2018-11-07T10:04:08Z"],["dc.date.issued","2015"],["dc.description.abstract","Ethanol inhibits memory encoding and the induction of long-term potentiation (LTP) in CA1 neurons of the hippocampus. Hippocampal LTP at Schaffer collateral synapses onto CA1 pyramidal neurons has been widely studied as a cellular model of learning and memory, but there is striking heterogeneity in the underlying molecular mechanisms in distinct regions and in response to distinct stimuli. Basal and apical dendrites differ in terms of innervation, input specificity, and molecular mechanisms of LTP induction and maintenance, and different stimuli determine distinct molecular pathways of potentiation. However, lamina or stimulus-dependent effects of ethanol on LTP have not been investigated. Here, we tested the effect of acute application of 60 mM ethanol on LTP induction in distinct dendritic compartments (apical versus basal) of CA1 neurons, and in response to distinct stimulation paradigms (single versus repeated, spaced high frequency stimulation). We found that ethanol completely blocks LTP in apical dendrites, whereas it reduces the magnitude of LTP in basal dendrites. Acute ethanol treatment for just 15 min altered pre- and post-synaptic protein expression. Interestingly, ethanol increases the neurosteroid allopregnanolone, which causes ethanol-dependent inhibition of LTP, more prominently in apical dendrites, where ethanol has greater effects on LTP. This suggests that ethanol has general effects on fundamental properties of synaptic plasticity, but the magnitude of its effect on LTP differs depending on hippocampal sub-region and stimulus strength. (c) 2014 Wiley Periodicals, Inc."],["dc.identifier.doi","10.1002/hipo.22356"],["dc.identifier.isi","000346255600010"],["dc.identifier.pmid","25155179"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38630"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-1063"],["dc.relation.issn","1050-9631"],["dc.title","Ethanol Inhibits Long-Term Potentiation in Hippocampal CA1 Neurons, Irrespective of Lamina and Stimulus Strength, Through Neurosteroidogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","eaav1483"],["dc.bibliographiccitation.issue","6422"],["dc.bibliographiccitation.journal","Science (New York, N.Y.)"],["dc.bibliographiccitation.volume","363"],["dc.contributor.author","Awasthi, Ankit"],["dc.contributor.author","Ramachandran, Binu"],["dc.contributor.author","Ahmed, Saheeb"],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Shinoda, Yo"],["dc.contributor.author","Nitzan, Noam"],["dc.contributor.author","Heukamp, Alina"],["dc.contributor.author","Rannio, Sabine"],["dc.contributor.author","Martens, Henrik"],["dc.contributor.author","Barth, Jonas"],["dc.contributor.author","Burk, Katja"],["dc.contributor.author","Wang, Yu Tian"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Dean, Camin"],["dc.date.accessioned","2019-07-31T13:02:46Z"],["dc.date.available","2019-07-31T13:02:46Z"],["dc.date.issued","2019"],["dc.description.abstract","Forgetting is important. Without it, the relative importance of acquired memories in a changing environment is lost. We discovered that synaptotagmin-3 (Syt3) localizes to postsynaptic endocytic zones and removes AMPA receptors from synaptic plasma membranes in response to stimulation. AMPA receptor internalization, long-term depression (LTD), and decay of long-term potentiation (LTP) of synaptic strength required calcium-sensing by Syt3 and were abolished through Syt3 knockout. In spatial memory tasks, mice in which Syt3 was knocked out learned normally but exhibited a lack of forgetting. Disrupting Syt3:GluA2 binding in a wild-type background mimicked the lack of LTP decay and lack of forgetting, and these effects were occluded in the Syt3 knockout background. Our findings provide evidence for a molecular mechanism in which Syt3 internalizes AMPA receptors to depress synaptic strength and promote forgetting."],["dc.identifier.doi","10.1126/science.aav1483"],["dc.identifier.pmid","30545844"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62245"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1095-9203"],["dc.relation.issn","0036-8075"],["dc.relation.issn","1095-9203"],["dc.title","Synaptotagmin-3 drives AMPA receptor endocytosis, depression of synapse strength, and forgetting"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["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","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"]]