Chronic membrane depolarization regulates the level of the guanine nucleotide binding protein G(o)α in cultured neuronal cells

Charles W Luetje, N. M. Nathanson

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Chronic membrane depolarization results in an increase in muscarinic acetylcholine receptor (mAChR) number in N1E-115 neuroblastoma cells. Because the mAChR interacts with the guanine nucleotide binding regulatory (G) proteins, G(i) and G(o), the effect of chronic membrane depolarization on the levels of subunits of these G proteins was examined. Quantitation of G protein subunit levels was performed using affinity-purified, monospecific antibodies in quantitative immunoblot assay. Incubation with 50 μM veratridine (VTN), an activator of voltage-sensitive Na+ channels, induced a 48 ± 15% increase in the level of the α subunit of G(o). The effect of VTN was blocked by tetrodotoxin. On removal of VTN, the level of G(o)α decreased to control levels within 24 h. The levels of the α subunit of G(i) and the common β subunit were not affected by VTN treatment. These results show that in N1E-115 cells, the level of the α subunit of G(o) is regulated in a manner similar to the level of mAChR in response to chronic membrane depolarization.

Original languageEnglish
Pages (from-to)1775-1782
Number of pages8
JournalJournal of Neurochemistry
Volume50
Issue number6
StatePublished - Jan 1 1988
Externally publishedYes

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Veratridine
Guanine Nucleotides
Depolarization
Cultured Cells
Carrier Proteins
Muscarinic Receptors
GTP-Binding Proteins
Membranes
Level control
Tetrodotoxin
Protein Subunits
Neuroblastoma
Assays
Antibodies
Electric potential

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

Chronic membrane depolarization regulates the level of the guanine nucleotide binding protein G(o)α in cultured neuronal cells. / Luetje, Charles W; Nathanson, N. M.

In: Journal of Neurochemistry, Vol. 50, No. 6, 01.01.1988, p. 1775-1782.

Research output: Contribution to journalArticle

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