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.