Journal Article (Review Article) DZNE-2020-06577

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Do TRPC channels support working memory? Comparing modulations of TRPC channels and working memory through G-protein coupled receptors and neuromodulators.

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2018
Elsevier Amsterdam

Behavioural brain research 354, 64-83 () [10.1016/j.bbr.2018.02.042]

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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.

Keyword(s): Acetylcholine: physiology (MeSH) ; Action Potentials (MeSH) ; Animals (MeSH) ; Conditioning, Psychological (MeSH) ; Dopamine: physiology (MeSH) ; Hippocampus: physiology (MeSH) ; Humans (MeSH) ; Memory, Short-Term: physiology (MeSH) ; Neurons: physiology (MeSH) ; Norepinephrine: physiology (MeSH) ; Receptors, G-Protein-Coupled: physiology (MeSH) ; Serotonin: physiology (MeSH) ; TRPC Cation Channels: physiology (MeSH) ; Receptors, G-Protein-Coupled ; TRPC Cation Channels ; Serotonin ; Acetylcholine ; Dopamine ; Norepinephrine

Classification:

Contributing Institute(s):
  1. Cognitive Neurophysiology (AG Yoshida)
  2. Functional Neuroimaging (AG Angenstein)
Research Program(s):
  1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)
  2. 344 - Clinical and Health Care Research (POF3-344) (POF3-344)

Appears in the scientific report 2018
Database coverage:
Medline ; BIOSIS Previews ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF < 5 ; JCR ; NationallizenzNationallizenz ; SCOPUS ; Web of Science Core Collection
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Document types > Articles > Journal Article
Institute Collections > MD DZNE > MD DZNE-AG Angenstein
Institute Collections > MD DZNE > MD DZNE-AG Yoshida
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 Record created 2020-02-18, last modified 2024-03-21


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