J 2018

Association between genetic variability of neuronal nitric oxide synthase and sensorimotor gating in humans

ROVNY, Rastislav, Martin MARKO, Stanislav KATINA, Jana MURINOVA, Veronika ROHARIKOVA et. al.

Basic information

Original name

Association between genetic variability of neuronal nitric oxide synthase and sensorimotor gating in humans

Authors

ROVNY, Rastislav (703 Slovakia), Martin MARKO (703 Slovakia), Stanislav KATINA (703 Slovakia, belonging to the institution), Jana MURINOVA (703 Slovakia), Veronika ROHARIKOVA (703 Slovakia), Barbora CIMROVA (703 Slovakia), Gabriela REPISKA (703 Slovakia), Gabriel MINARIK (703 Slovakia) and Igor RIECANSKY (703 Slovakia, guarantor)

Edition

NITRIC OXIDE-BIOLOGY AND CHEMISTRY, Rochester, USA, Elsevier, 2018, 1089-8603

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

10103 Statistics and probability

Country of publisher

United States of America

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

Impact factor

Impact factor: 3.371

RIV identification code

RIV/00216224:14310/18:00103407

Organization unit

Faculty of Science

UT WoS

000448231800004

Keywords in English

Nitric oxide; NOS1; Schizophrenia; Prepulse inhibition; Startle; Endophenotypes

Tags

International impact, Reviewed
Změněno: 8/4/2020 12:18, Mgr. Marie Šípková, DiS.

Abstract

V originále

Research increasingly suggests that nitric oxide (NO) plays a role in the pathogenesis of schizophrenia. One important line of evidence comes from genetic studies, which have repeatedly detected an association between the neuronal isoform of nitric oxide synthase (nNOS or NOS1) and schizophrenia. However, the pathogenetic pathways linking nNOS, NO, and the disorder remain poorly understood. A deficit in sensorimotor gating is considered to importantly contribute to core schizophrenia symptoms such as psychotic disorganization and thought disturbance. We selected three candidate nNOS polymorphisms (Ex1f-VNTR, rs6490121 and rs41279104), associated with schizophrenia and cognition in previous studies, and tested their association with the efficiency of sensorimotor gating in healthy human adults. We found that risk variants of Ex1f-VNTR and rs6490121 (but not rs41279104) were associated with a weaker prepulse inhibition (PPI) of the acoustic startle reflex, a standard measure of sensorimotor gating. Furthermore, the effect of presence of risk variants in Ex1f- VNTR and rs6490121 was additive: PPI linearly decreased with increasing number of risk alleles, being highest in participants with no risk allele, while lowest in individuals who carry three risk alleles. Our findings indicate that NO is involved in the regulation of sensorimotor gating, and highlight one possible pathogenetic mechanism for NO playing a role in the development of schizophrenia psychosis.