Neuronal-type acetylcholine receptors and regulation of ?7 gene expression in vertebrate skeletal muscle

✍ Scribed by Romano, Suzanne J. ;Pugh, Phyllis C. ;McIntosh, J. Michael ;Berg, Darwin K.

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 149 KB
• Volume: 32
• Category: Article
• ISSN: 0022-3034
• DOI: 10.1002/(sici)1097-4695(199701)32:1<69::aid-neu7>3.0.co;2-c

✦ Synopsis

Several neuronal nicotinic acetylnumber. Similarly, treating myotube cultures with techoline receptor (AChR) genes are expressed in chick trodotoxin caused a modest increase in a7 transcript skeletal muscle during development. One of the most levels and a large increase in a1. Calcitonin geneabundantly expressed is a7, which produces a protein related peptide (CGRP) increased both kinds of trancapable of binding a-bungarotoxin and is physically scripts in myotube cultures equally as did treatment distinct from muscle AChRs containing the a1 gene with 8-bromo-cyclic AMP; CGRP is thought to work product. We show here that the a7-containing species via a cyclic AMP-dependent pathway in muscle. In at in muscle is indistinguishable pharmacologically from least one respect, however, a7 expression in muscle a7-containing AChRs in neurons. In addition, immudiffers qualitatively from that of a1: AChR-inducing nologic analysis with subunit-specific muscle antibodactivity (ARIA) increased a1 mRNA levels in culture ies shows that the a7-containing species in muscle while slightly depressing a7 mRNA levels. The regulalacks the b1 and d muscle AChR gene products as it tory pattern of a7 expression in muscle may combine does the a1. RNase protection experiments measuring features of both a7 expression in neurons and a1 ex-a7 mRNA levels indicate that the a1 and a7 genes pression in muscle.