Role for calcium from the sarcoplasmic reticulum in coupling muscle activity to nicotinic acetylcholine receptor gene expression in rat
✍ Scribed by Adams, Larry ;Goldman, Daniel
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 189 KB
- Volume
- 35
- Category
- Article
- ISSN
- 0022-3034
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✦ Synopsis
subunit RNA levels as a result of decreasing nAChR ABSTRACT: Neurally evoked muscle electrical subunit promoter activity. Finally, we show that this activity suppresses nicotinic acetylcholine receptor decreased promoter activity is mediated through the (nAChR) gene expression in extrajunctional domains same DNA sequences that control activity-dependent of adult muscle fibers. It has been proposed that this gene expression. Therefore, we propose that in rat regulation is mediated by calcium influx through voltmuscle, calcium release from the SR participates in age-dependent L-type calcium channels but bypasses coupling muscle depolarization to nAChR gene the sarcoplasmic reticulum in chick and mouse C2C12 expression. ᭧ 1998 John Wiley & Sons, Inc. J Neurobiol 35: 245- cells. Here we report that in rat muscle calcium influx 257, 1998 through L-type calcium channels preferentially re-Keywords: muscle; nicotinic acetylcholine receptor; duced nAChR 1-subunit RNA via a post-transcripactivity-dependent gene expression; calcium; sarcotional mechanism. In contrast, calcium release from plasmic reticulum the sarcoplasmic reticulum (SR) suppressed nAChR