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@ARTICLE{Reboreda:140255,
      author       = {Reboreda, Antonio and Theissen, Frederik M and
                      Valero-Aracama, Maria J and Arboit, Alberto and Corbu,
                      Mihaela A and Yoshida, Motoharu},
      title        = {{D}o {TRPC} channels support working memory? {C}omparing
                      modulations of {TRPC} channels and working memory through
                      {G}-protein coupled receptors and neuromodulators.},
      journal      = {Behavioural brain research},
      volume       = {354},
      issn         = {0166-4328},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-06577},
      pages        = {64-83},
      year         = {2018},
      abstract     = {Working memory is a crucial ability we use in daily life.
                      However, the cellular mechanisms supporting working memory
                      still remain largely unclear. A key component of working
                      memory is persistent neural firing which is believed to
                      serve short-term (hundreds of milliseconds up to tens of
                      seconds) maintenance of necessary information. In this
                      review, we will focus on the role of transient receptor
                      potential canonical (TRPC) channels as a mechanism
                      underlying persistent firing. Many years of in vitro work
                      have been suggesting a crucial role of TRPC channels in
                      working memory and temporal association tasks. If TRPC
                      channels are indeed a central mechanism for working memory,
                      manipulations which impair or facilitate working memory
                      should have a similar effect on TRPC channel modulation.
                      However, modulations of working memory and TRPC channels
                      were never systematically compared, and it remains
                      unanswered whether TRPC channels indeed contribute to
                      working memory in vivo or not. In this article, we review
                      the effects of G-protein coupled receptors (GPCR) and
                      neuromodulators, including acetylcholine, noradrenalin,
                      serotonin and dopamine, on working memory and TRPC channels.
                      Based on comparisons, we argue that GPCR and downstream
                      signaling pathways that activate TRPC, generally support
                      working memory, while those that suppress TRPC channels
                      impair it. However, depending on the channel types, areas,
                      and systems tested, this is not the case in all studies.
                      Further work to clarify involvement of specific TRPC
                      channels in working memory tasks and how they are affected
                      by neuromodulators is still necessary in the future.},
      subtyp        = {Review Article},
      keywords     = {Acetylcholine: physiology / Action Potentials / Animals /
                      Conditioning, Psychological / Dopamine: physiology /
                      Hippocampus: physiology / Humans / Memory, Short-Term:
                      physiology / Neurons: physiology / Norepinephrine:
                      physiology / Receptors, G-Protein-Coupled: physiology /
                      Serotonin: physiology / TRPC Cation Channels: physiology /
                      Receptors, G-Protein-Coupled (NLM Chemicals) / TRPC Cation
                      Channels (NLM Chemicals) / Serotonin (NLM Chemicals) /
                      Acetylcholine (NLM Chemicals) / Dopamine (NLM Chemicals) /
                      Norepinephrine (NLM Chemicals)},
      cin          = {AG Yoshida / AG Angenstein},
      ddc          = {610},
      cid          = {I:(DE-2719)1310011 / I:(DE-2719)1310004},
      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},
      pubmed       = {pmid:29501506},
      doi          = {10.1016/j.bbr.2018.02.042},
      url          = {https://pub.dzne.de/record/140255},
}