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@ARTICLE{Arboit:151515,
      author       = {Arboit, Alberto and Reboreda, Antonio and Yoshida,
                      Motoharu},
      title        = {{I}nvolvement of {TRPC}4 and 5 {C}hannels in {P}ersistent
                      {F}iring in {H}ippocampal {CA}1 {P}yramidal {C}ells},
      journal      = {Cells},
      volume       = {9},
      number       = {2},
      issn         = {2073-4409},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DZNE-2020-01099},
      pages        = {365},
      year         = {2020},
      abstract     = {Persistent neural activity has been observed in vivo during
                      working memory tasks, and supports short-term (up to tens of
                      seconds) retention of information. While synaptic and
                      intrinsic cellular mechanisms of persistent firing have been
                      proposed, underlying cellular mechanisms are not yet fully
                      understood. In vitro experiments have shown that individual
                      neurons in the hippocampus and other working memory related
                      areas support persistent firing through intrinsic cellular
                      mechanisms that involve the transient receptor potential
                      canonical (TRPC) channels. Recent behavioral studies
                      demonstrating the involvement of TRPC channels on working
                      memory make the hypothesis that TRPC driven persistent
                      firing supports working memory a very attractive one.
                      However, this view has been challenged by recent findings
                      that persistent firing in vitro is unchanged in TRPC knock
                      out (KO) mice. To assess the involvement of TRPC channels
                      further, we tested novel and highly specific TRPC channel
                      blockers in cholinergically induced persistent firing in
                      mice CA1 pyramidal cells for the first time. The application
                      of the TRPC4 blocker ML204, TRPC5 blocker clemizole
                      hydrochloride, and TRPC4 and 5 blocker Pico145, all
                      significantly inhibited persistent firing. In addition,
                      intracellular application of TRPC4 and TRPC5 antibodies
                      significantly reduced persistent firing. Taken together
                      these results indicate that TRPC4 and 5 channels support
                      persistent firing in CA1 pyramidal neurons. Finally, we
                      discuss possible scenarios causing these controversial
                      observations on the role of TRPC channels in persistent
                      firing.},
      keywords     = {Action Potentials: drug effects / Action Potentials:
                      physiology / Animals / Antibodies: pharmacology /
                      Benzimidazoles: pharmacology / CA1 Region, Hippocampal: drug
                      effects / CA1 Region, Hippocampal: physiology / Cholinergic
                      Agonists: pharmacology / Indoles: pharmacology / Male / Mice
                      / Neurons: drug effects / Neurons: physiology / Piperidines:
                      pharmacology / Pyramidal Cells: drug effects / Pyramidal
                      Cells: physiology / TRPC Cation Channels: antagonists $\&$
                      inhibitors / TRPC Cation Channels: metabolism},
      cin          = {AG Angenstein / AG Yoshida},
      ddc          = {570},
      cid          = {I:(DE-2719)1310004 / I:(DE-2719)1310011},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 344
                      - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC7072216},
      pubmed       = {pmid:32033274},
      doi          = {10.3390/cells9020365},
      url          = {https://pub.dzne.de/record/151515},
}