Exclusion of close linkage of bipolar disorder to the Gs-α subunit gene in nine Australian pedigrees

F. Le, P. Mitchell*, C. Vivero, B. Waters, J. Donald, L. A. Selbie, J. Shine, P. Schofield

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

32 Citations (Scopus)


Growing evidence suggests that guanine nucleotide binding proteins (G proteins) may be involved in both the pathogenesis and treatment of bipolar affective disorder. Both overactive G proteins and increased levels of the α subunit of the stimulatory form (Gs-α) have been demonstrated in peripheral leucocytes of manic patients while an increase of Gs-α subunit levels has also been found in a postmortem study of bipolar disorder. The function of Gs and Gi α subunits has now been shown to be affected by lithium. The present study aimed to determine whether bipolar affective disorder was linked to the Gs-α subunit gene which has been mapped to chromosomal region 20q13.2. Linkage analysis utilized the PCR amplification of a portion of the Gs-α gene that contains a dinucleotide repeat (CA repeat) polymorphism. Linkage of bipolar disorder and recurrent depression to the Gs-α subunit gene was tested using a series of autosomal dominant and recessive models with varying penetrance levels. Additionally, linkage was examined using a series of levels of definitions of affective illness. Close linkage to the Gs-α subunit gene was strongly excluded using each model and definition. Thus, our study indicates that a genetic defect in the Gs-α subunit gene is unlikely to be the cause of bipolar disorder.

Original languageEnglish
Pages (from-to)187-195
Number of pages9
JournalJournal of Affective Disorders
Issue number3
Publication statusPublished - 1994
Externally publishedYes


  • Bipolar disorder
  • Chromosome 20
  • G protein
  • G-α
  • Linkage analysis


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