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Cited by 364

The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.

Suppression of inflammatory and neuropathic pain symptoms in mice lacking the N-type Ca2+ channel

Open access
Saegusa, H.·2001·The EMBO Journal

Abstract

The importance of voltage-dependent Ca2+ channels (VDCCs) in pain transmission has been noticed gradually, as several VDCC blockers have been shown to be effective in inhibiting this process. In particular, the N-type VDCC has attracted attention, because inhibitors of this channel are effective in various aspects of pain-related phenomena. To understand the genuine contribution of the N-type VDCC to the pain transmission system, we generated mice deficient in this channel by gene targeting. We report here that mice lacking N-type VDCCs show suppressed responses to a painful stimulus that induces inflammation and show markedly reduced symptoms of neuropathic pain, which is caused by nerve injury and is known to be difficult to treat by currently available therapeutic methods. This finding clearly demonstrates that the N-type VDCC is essential for development of neuropathic pain and, therefore, controlling the activity of this channel can be of great importance for the management of neuropathic pain.

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Metadata

Authors
Saegusa, H.
Venue
The EMBO Journal
Published
2001-05-15
Volume
20
Issue
10
Pages
2349-2356
ISSN
  • 0261-4189 (ISSN-L)
  • 1460-2075
OpenAlex
W1965547314
Cited by
364
References
41
FWCI
7.92
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Suppression of inflammatory and neuropathic pain symptoms in mice lacking the N-type Ca2+ channel. https://app.cochat.ai/papers/10.1093/emboj/20.10.2349
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Saegusa, H. (2001). Suppression of inflammatory and neuropathic pain symptoms in mice lacking the N-type Ca2+ channel. The EMBO Journal. https://doi.org/10.1093/emboj/20.10.2349

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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