Chronic stimulation differentially modulates expression of mRNA for dihydropyridine receptor isoforms in rat fast twitch skeletal muscle

Yann Péréon, Javier Navarro, Marc Hamilton, Frank W. Booth, Philip Palade

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

This study examined the effects of low frequency chronic stimulation on expression of the mRNA encoding the two isoforms of the α1 subunit of the dihydropyridine receptor (DHPR) calcium channel, a critical component of skeletal muscle excitation-contraction coupling. RNase protection assay was used to determine alteration in isoform expression in 5-day, 9-day and 13-day chronically stimulated rat tibialis anterior muscle, and to compare it with soleus and extensor digitorum longus muscles. Low frequency chronic stimulation was associated not only with a significant decrease in the mRNA level of the skeletal isoform of the DHPR, but also with a significant increase in the mRNA level of the cardiac isoform of the DHPR, the overwhelming majority of which was the adult splice variant. Significant levels of cardiac DHPR mRNA expression were also found in normal adult slow twitch soleus muscle. These findings raise the question of a potential role for the cardiac DHPR in certain adult skeletal muscles.

Original languageEnglish
Pages (from-to)217-222
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume235
Issue number1
DOIs
StatePublished - Jun 9 1997

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L-Type Calcium Channels
Muscle
Rats
Protein Isoforms
Skeletal Muscle
Messenger RNA
Excitation Contraction Coupling
Muscles
Calcium Channels
Ribonucleases
Muscle Contraction
Assays

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

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Chronic stimulation differentially modulates expression of mRNA for dihydropyridine receptor isoforms in rat fast twitch skeletal muscle. / Péréon, Yann; Navarro, Javier; Hamilton, Marc; Booth, Frank W.; Palade, Philip.

In: Biochemical and Biophysical Research Communications, Vol. 235, No. 1, 09.06.1997, p. 217-222.

Research output: Contribution to journalArticle

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