CACNA1C risk variant and amygdala activity in bipolar disorder, schizophrenia and healthy controls

PLoS One. 2013;8(2):e56970. doi: 10.1371/journal.pone.0056970. Epub 2013 Feb 20.

Abstract

Objectives: Several genetic studies have implicated the CACNA1C SNP rs1006737 in bipolar disorder (BD) and schizophrenia (SZ) pathology. This polymorphism was recently found associated with increased amygdala activity in healthy controls and patients with BD. We performed a functional Magnetic Resonance Imaging (fMRI) study in a sample of BD and SZ cases and healthy controls to test for altered amygdala activity in carriers of the rs1006737 risk allele (AA/AG), and to investigate if there were differences across the diagnostic groups.

Methods: Rs1006737 was genotyped in 250 individuals (N = 66 BD, 61 SZ and 123 healthy controls), all of Northern European origin, who underwent an fMRI negative faces matching task. Statistical tests were performed with a model correcting for sex, age, diagnostic category and medication status in the total sample, and then in each diagnostic group.

Results: In the total sample, carriers of the risk allele had increased activation in the left amygdala. Group-wise analyses showed that this effect was significant in the BD group, but not in the other diagnostic groups. However, there was no significant interaction effect for the risk allele between BD and the other groups.

Conclusions: These results indicate that CACNA1C SNP rs1006737 affects amygdala activity during emotional processing across all diagnostic groups. The current findings add to the growing body of knowledge of the pleiotropic effect of this polymorphism, and further support that ion channel dysregulation is involved in the underlying mechanisms of BD and SZ.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Amygdala / pathology
  • Amygdala / physiopathology*
  • Bipolar Disorder / diagnosis
  • Bipolar Disorder / genetics*
  • Bipolar Disorder / physiopathology*
  • Calcium Channels, L-Type / genetics*
  • Humans
  • Magnetic Resonance Imaging
  • Polymorphism, Single Nucleotide
  • Psychomotor Performance
  • Reaction Time
  • Schizophrenia / diagnosis
  • Schizophrenia / genetics*
  • Schizophrenia / physiopathology*

Substances

  • CACNA1C protein, human
  • Calcium Channels, L-Type

Grants and funding

The study was supported by grants to the TOP study group from the University of Oslo (http://www.uio.no/english/), the Research Council of Norway (http://www.forskningsradet.no/servlet/Satellite?c=Page&cid=1177315753906&p=1177315753906&pagename=ForskningsradetEngels%2FHovedsidemal) (#167153/V50, #163070/V50) and the SouthEast Norway Health Authority (http://www.helse-sorost.no/omoss/english/Sider/page.aspx) (#2004123, #2008-080). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.