Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Scientific Correspondence
  • Published:

Analysis of structural polymorphisms and C-1018G promoter variant of the 5-HT1A receptor gene as putative risk factors in major depression

Molecular Psychiatry volume 7, pages 930–932 (2002)Cite this article

An Erratum to this article was published on 27 February 2003

SIR – Alterations in the serotonergic system have been related to the origin of depression. The serotonin 1A receptor gene is a strong candidate for major depression because of involvement in antidepressant response and control of intersynaptic serotonin release. Genetic alterations in the 5-HT1A gene may be related to the receptor involvement in depression. A sample of 249 patients with major depression and 170 controls were analysed for four different polymorphisms of the 5-HT1A receptor gene. No differences in genotype or allele frequencies were found between patients and controls. Our results suggest that genetic variability in the 5-HT1A receptor gene does not play a major role in the aetiology of major depression.

Serotonin neurotransmission is involved in the regulation of mood, sleep, vigilance, memory and learning, feeding and sexual behaviour. All those functions have found to be altered to varying extents in depressed patients. The serotonin 1A receptor has been postulated as playing a major role in anxiety, depression and other psychiatric disorders.1 This receptor regulates the firing of serotonergic neurones and mediates the action of non-serotonergic neurones prominently in the limbic regions.2 Moreover, the 5-HT1A receptor has been hypothesised to have an important role in the modulation of clinical response to antidepressant drugs. Long-term treatment with SSRIs desensitises the somatodendritic 5-HT1A receptors leading to an enhanced release of serotonin.3 In addition, it has been reported that a combination of SSRI drugs and blockade of these receptors may accelerate the therapeutic efficacy in depressive patients.4 All these facts lead us to consider the 5-HT1A receptor gene as a good candidate gene for association studies in major depression. The 5-HT1A receptor gene (chromosome 15q11) is intronless and codes a 422-amino acid protein.5 A number of low frequency single nucleotide polymorphisms (SNPs) have been described on this gene.6,7 Previous association studies investigating the putative role of the 5-HT1Areceptor gene in schizophrenia and major depression have failed to demonstrate any relation between these polymorphisms and the disorders.6,7,8

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

References

  1. Hammon M . In: Baumgarter HG, Gethert M (ed) Serotoninergic Neurons and 5HT Receptors in the CNS Springer: Heidelberg 1997 pp 239–268

    Google Scholar 

  2. Dubovsky SL, Thomas M . J Clin Psychiatry 1995 55 (Suppl): 38–48

  3. Artigas F et al. Trends Neurosci 1996 19: 378–383

  4. Zanardi R et al. J Clin Psychopharmacol 1997 17: 446–450

  5. Kobilka BK et al. Nature 1987 329: 75–79

  6. Kawanishi Y et al. Am J Med Gen (Neuropsych Genet) 1998 81: 434–439

  7. Erdmann J et al. Am J Med Gen 1995 60: 393–399

  8. Serretti A et al. Am J Med Genet 2000 96: 161–166

  9. Wu S, Comings DE . Psychiatr Genet 1999 9: 105–106

  10. American Psychiatric Association. DUMMY ARTICLE. Diagnostic and Statistical Manual of Mental Disorders, 4th edn American Psychiatric Association: Washington, DC 1994

  11. Spitzer RL et al. DUMMY ARTICLE. Structured Clinical Interview for DSM-III R American Psychiatric Press: Washington DC 1990

    Google Scholar 

  12. Gutierrez B et al. Hum Genet 1998 103: 319–322

  13. Arias B et al. Mol Psychiatry 2001 6: 239–242

  14. Arias B et al. Am J Med Genet 2001 105: 801–805

Download references

Author information

Authors and Affiliations

  1. Unitat d'Antropologia, Departament de Biologia Animal, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain

    B Arias, B Gutierrez & L Fananas

  2. Centre de Salut Mental Esquerre de l'Eixample, Hospital Clínic i Provincial de Barcelona, Spain

    C Gasto, R Catalan & L Pintor

  3. Institut d'Investigació Biomèdica Agustí Pi i Suner (IDIBAPS),

    C Gasto, R Catalan & L Pintor

  4. Division of Psychological Medicine, Clinical Neuropharmacology, Institute of Psychiatry, London, UK

    M J Arranz & R W Kerwin

Authors
  1. B Arias
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. M J Arranz
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. C Gasto
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. R Catalan
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. L Pintor
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. B Gutierrez
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. R W Kerwin
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. L Fananas
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to L Fananas.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Arias, B., Arranz, M., Gasto, C. et al. Analysis of structural polymorphisms and C-1018G promoter variant of the 5-HT1A receptor gene as putative risk factors in major depression. Mol Psychiatry 7, 930–932 (2002). https://doi.org/10.1038/sj.mp.4001146

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/sj.mp.4001146

This article is cited by

Search

Advanced search

Quick links