Cited by 42Ion channel regulation and functionNeuroscience and Neuropharmacology ResearchProtein Kinase Regulation and GTPase Signaling

Excitation–transcription coupling in sympathetic neurons and the molecular mechanism of its initiation

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Ma, Huan, Groth, Rachel D., Wheeler, Damian G., Barrett, Curtis F., Tsien, Richard W.·2011·Neuroscience Research

Abstract

In excitable cells, membrane depolarization and activation of voltage-gated Ca²+ (Ca(V)) channels trigger numerous cellular responses, including muscle contraction, secretion, and gene expression. Yet, while the mechanisms underlying excitation-contraction and excitation-secretion coupling have been extensively characterized, how neuronal activity is coupled to gene expression has remained more elusive. In this article, we will discuss recent progress toward understanding the relationship between patterns of channel activity driven by membrane depolarization and activation of the nuclear transcription factor CREB. We show that signaling strength is steeply dependent on membrane depolarization and is more sensitive to the open probability of Ca(V) channels than the Ca²+ entry itself. Furthermore, our data indicate that by decoding Ca(V) channel activity, CaMKII (a Ca²+/calmodulin-dependent protein kinase) links membrane excitation to activation of CREB in the nucleus. Together, these results revealed some interesting and unexpected similarities between excitation-transcription coupling and other forms of excitation-response coupling.

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Crossref · 10.1016/j.neures.2011.02.004

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  • The Guenthner study used a genetic labeling technique nearly identical to ours, but recombination was driven by promoters for immediate-early genes Fos and Arc, upregulated as part of excitation-transcription neuronal response to synaptic activity initiated by CREB phosphorylation.

    “The Guenthner study [9] used a genetic labeling technique nearly identical to ours, but recombination was driven by promoters for the immediate-early genes Fos and Arc, upregulated as part of the “excitation-transcription” neuronal response to synaptic activity initiated by CREB phosphorylation [40].”

    From Tamoxifen induces cellular stress in the nervous system by inhibiting cholesterol synthesis (2015) · cites this paper as [40]

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  1. Jenkins MA Christel CJ Jiao Y Abiria S Kim KY Usachev YM Obermair GJ Colbran RJ Lee A 2010 Ca2+-dependent facilitation of Cav1.3 Ca2+ channels by densin and Ca2+/calmodulin-dependent protein kinase II J Neurosci 30 5125 5135 20392935 PMC2990970

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Authors
Ma, H., Groth, R. D., Wheeler, D. G., Barrett, C. F., & Tsien, R. W.
Affiliations
Stanford Medicine (US)
Corresponding author
Tsien, Richard W.
Venue
Neuroscience Research
Publisher
Elsevier BV
Published
2011-05
Volume
70
Issue
1
Pages
2-8
ISSN
0168-0102 (ISSN-L)
OpenAlex
W1987938334
Cited by
42
References
48
Citations by year
2025: 3 · 2024: 2 · 2023: 1 · 2021: 2 · 2020: 2 · 2019: 3 · 2018: 3 · 2017: 10 · 2016: 1 · 2015: 7 · 2014: 2 · 2013: 2 · 2012: 3
FWCI
0.23
Type
journal article
Language
en
Open access
Locations
  • Neuroscience Research (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute of General Medical Sciences
  • National Institute of Neurological Disorders and Stroke
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Keywords
excitation-transcription coupling, sympathetic neurons, voltage-gated calcium channels, CREB, CaMKII, membrane depolarization, calcium signaling, gene expression
MeSH terms
Action Potentials, Animals, Ganglia, Sympathetic, Humans, Neurons, Calcium Channels, Calcium Signaling

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