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World J Biol Psychiatry. 2011 Aug;12(5):376-84. doi: 10.3109/15622975.2011.552192. Epub 2011 May 19.

Sensory gating deficit is associated with catechol-O-methyltransferase polymorphisms in bipolar disorder.

Author information

1
Laboratory of Psychoneuroendocrinology and Molecular Genetics. Biomedical Research Foundation, Clínico San Carlos Hospital, Madrid, Spain.

Abstract

OBJECTIVES:

Recent studies have evidenced that bipolar patients show a sensory gating deficit (P50). Among the neural systems that could be influencing this electrophysiological phenotype, dopamine seems to play an important role. We hypothesize that catechol-O-methyltransferase (COMT), the main metabolizer of dopamine in prefrontal cortex, is related to this deficit.

METHODS:

We selected three polymorphisms in COMT gene: rs2075507 (Promoter 2 region), Val158Met (rs4680) and rs165599 (3' region). A case-control study was performed in 784 controls and 238 bipolar patients. Besides, 122 euthymic bipolar subjects and 95 healthy subjects carried out a sensory gating task (P50).

RESULTS:

Polymorphism rs165599 in the COMT gene was associated with susceptibility to bipolar disorder (BD), mainly in women (AG: OR = 1.46; GG: OR = 1.84; P = 0.03). In the female group, haplotype AAG was associated with an OR = 7.6. Subjects who carried Val158 allele evidenced a deficit in suppression (P = 0.046) and rs165599 allele G carriers (mainly in homozygosis) had a bigger S2 amplitude and a higher S2/S1 ratio (1.6(e-5) < P < 0.01). Not a single association was proven in the control group.

CONCLUSIONS:

Our results support the association of the COMT gene with BD and with one of its potential endophenotypes, auditory sensory gating deficit, measured by the P50 paradigm.

PMID:
21595525
DOI:
10.3109/15622975.2011.552192
[Indexed for MEDLINE]

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