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.

Základní údaje

Originální název

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

Autoři

ROVNY, Rastislav (703 Slovensko), Martin MARKO (703 Slovensko), Stanislav KATINA (703 Slovensko, domácí), Jana MURINOVA (703 Slovensko), Veronika ROHARIKOVA (703 Slovensko), Barbora CIMROVA (703 Slovensko), Gabriela REPISKA (703 Slovensko), Gabriel MINARIK (703 Slovensko) a Igor RIECANSKY (703 Slovensko, garant)

Vydání

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

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10103 Statistics and probability

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Odkazy

Impakt faktor

Impact factor: 3.371

Kód RIV

RIV/00216224:14310/18:00103407

Organizační jednotka

Přírodovědecká fakulta

UT WoS

000448231800004

Klíčová slova anglicky

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

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 8. 4. 2020 12:18, Mgr. Marie Šípková, DiS.

Anotace

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.