| Item type |
デフォルトアイテムタイプ_（フル）(1) |
| 公開日 |
2023-03-18 |
| タイトル |
|
|
タイトル |
Electrophysiological characterization of the tetrodotoxin-resistant Na + channel, Na v1.9, in mouse dorsal root ganglion neurons |
|
言語 |
en |
| 作成者 |
Maruyama, Hiroshi
Yamamoto, Mitsuko
Ohishi, Yoshiaki
Matsutomi, Tomoya
Zheng, Taixing
Nakata, Yoshihiro
Wood, John N.
Ogata, Nobukuni
|
| アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 権利情報 |
|
|
権利情報 |
Copyright (c) 2004 Springer-Verlag. "The original publication is available at www.springerlink.com" |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
Na channel |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
Dorsal root ganglion neuron |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
Tetrodotoxin |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
Patch-clamp |
| 主題 |
|
|
主題Scheme |
Other |
|
主題 |
Gating |
| 主題 |
|
|
主題Scheme |
NDC |
|
主題 |
490 |
| 内容記述 |
|
|
内容記述 |
The Na+ channel isoform, Navl.9 (NaN/SNS2), is preferentially expressed in small neurones of the dorsal root ganglia and thought to mediate a novel tetrodotoxin-resistant (TTX-R) Na+ current. We investigated properties of the Na+ current mediated by Nav1.9 (INaN) using whole-cell patch-clamp recording. To isolate INaN from a heterogeneous TTX-R Na+ current that also contained another type of TTX-R Na+ current mediated by Nay1.8 (SNS/PN3), we used Nay1.8-null mutant mice. Since F- that had been used as an internal anion in earlier studies was shown to produce negative shifts of the activation and inactivation kinetics of INaN, INaN was recorded with Cl- as an internal anion. The activation threshold for INaN was about 20 mV more negative than that for other Na+ currents, activation and inactivation were extremely slow giving rise to a persistent Na+ current, and the peak amplitude was too small (less than 0.5 nA) to carry an action potential generation. Thus, Nav1.9 is a 'background' Na+ channel that probably regulates excitability at a subthreshold voltage range and influences spike discharges that are predominantly mediated by other Na+ channels. Since functional expression of INaN declined with time after dissociation and recovered in step with concurrent glial outgrowth, Nav1.9 is an 'inducible' Na+ channel. Moreover, Nav1.9 is a 'kindling' Na+ channel, since the peak amplitude of INaN under whole cell patch clamp recording started to increase explosively after a variable period of delay, as if 'inactive' or 'silent' Nav1.9 channels were unmasked. Such an unusual increase of the current was not observed under nystatin-perforated recording and was prevented by ATP supplemented in the patch internal solution, indicating that the rupture of the patch membrane affected the normal behavior of Nav1.9. The inducible and kindling properties of INaN may provide an additional insight into the plasticity of Na+ channels that are related to pathological functions of Na+ channels accompanying abnormal pain states. |
|
言語 |
en |
| 出版者 |
|
|
出版者 |
Springer |
| 言語 |
|
|
言語 |
eng |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 出版タイプ |
|
|
出版タイプ |
AO |
|
出版タイプResource |
http://purl.org/coar/version/c_b1a7d7d4d402bcce |
| 関連情報 |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
10.1007/s00424-004-1315-0 |
| 関連情報 |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
http://dx.doi.org/10.1007/s00424-004-1315-0 |
| 収録物識別子 |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
0031-6768 |
| 収録物識別子 |
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|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA00771833 |
| 開始ページ |
|
|
開始ページ |
76 |
| 書誌情報 |
Pflügers Archiv : European Journal of Physiology
Pflügers Archiv : European Journal of Physiology
巻 449,
号 1,
p. 76-87,
発行日 2004-10
|
| 旧ID |
21538 |
EuroJPhys_449_76.pdf (1.7 MB)
