Evidence for the involvement of neuronal nitric oxide synthase and soluble guanylate cyclase on cognitive functions in rats

Çelikyurt, İpek Komşuoğlu; Göçmez, S.S.; Mutlu, Oğuz; Gacar, Nejat; Arıcıoğlu, Feyza; Utkan, Tijen

doi:10.1016/j.lfs.2011.09.017

Cited by 13 publications

(8 citation statements)

References 45 publications

(57 reference statements)

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“…Administering the drug just before the electrical shock can cause some nonspecific effects (e.g., analgesic effect, pain perception, and motility). Both ODQ (10 mg/kg) and 7-NI (15 mg/kg) treatment led to memory deterioration in the passive avoidance test in our study, in accordance with previous studies [28,37,43]. …”

Section: Discussionsupporting

confidence: 93%

Effects of 7-NI and ODQ on memory in the passive avoidance, novel object recognition, and social transmission of food preference tests in mice

Akar

Mutlu

Çelikyurt

et al. 2014

Med Sci Monit Basic Res

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BackgroundNitric oxide (NO) is an intercellular messenger that plays a critical role in learning and memory processes. Effects of nitric oxide synthase (NOS) inhibitors and guanylate cyclase (GC) inhibitors on cognitive function remain controversial.Material/MethodsThe aim of this study was to investigate effects of an NOS inhibitor, 7-nitroindazole (7-NI), and a GC inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), on different aspects of memory in passive avoidance (PA), novel object recognition (NOR), and social transmission of food preference (STFP) tests. Male Balb-c mice were treated intraperitoneally with 7-NI (15 mg/kg), ODQ (3,10 mg/kg), L-arginine (100 mg/kg) + 7-NI (15 mg/kg), or physiological saline.ResultsODQ (10 mg/kg) and 7-NI (15 mg/kg) significantly decreased second-day latency in PA test. 7-NI (15 mg/kg) and ODQ (10 mg/kg) significantly decreased the ratio index in the NOR test. 7-NI and ODQ (10 mg/kg) decreased cued/non-cued food eaten in STFP test. Amount of time spent in center zone significantly increased in ODQ (10 mg/kg) and 7-NI (15 mg/kg) groups in open field test, but there was no effect on total distance moved and speed of animals. ODQ (10 mg/kg) significantly increased number of entries into new compartments in exploratory activity apparatus, while 7-NI had no effect. Administration of L-arginine (100 mg/kg) before 7-NI reversed 7-NI-induced effects, supporting the role of NO in cognition.ConclusionsOur results confirm that inhibition of NO/cGMP/GS pathway might disturb emotional, visual, and olfactory memory in mice. Also, 7-NI and ODQ had anxiolytic effects in open field test, and ODQ also enhanced exploratory activity.

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Section: Discussionsupporting

confidence: 93%

Effects of 7-NI and ODQ on memory in the passive avoidance, novel object recognition, and social transmission of food preference tests in mice

Akar

Mutlu

Çelikyurt

et al. 2014

Med Sci Monit Basic Res

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“…The time course of different experimental manipulations used to study stages of memory are important [15]. It was reported that 3-Br 7-NI and ODQ disrupts reference and working memory processes by impairing strategies used for solving learning tasks, and, according to our results, nNOS-sGC may be required for emotional learning and reference and working memory [16]. …”

Section: Introductionsupporting

confidence: 61%

Effects of YC-1 on Learning and Memory Functions of Aged Rats

Çelikyurt

Utkan

Özer

et al. 2014

Med Sci Monit Basic Res

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BackgroundThe aim of this study was to investigate the effects of a potent nitric oxide-guanylate cyclase activator, 3-(5′-hydroxymethyl-2′-furyl)-1-benzylindazole (YC-1), on learning and memory functions in aged rats.Material/MethodsRats were divided into 2 groups as 4-month-old and 24-month-old rats. Rats received YC-1 (1 mg/kg/day) for 2 weeks long-term. Morris water maze (MWM) and passive avoidance (PA) tests were used to determine learning and memory functions.ResultsIn the MWM test, there is a significant increase in the acquisition latency (1–4 days) of 24-month-old rats. There is a significant reduction in the “time spent in the escape platform’s quadrant” in 24-month-old rats compared to 4-month-old rats in the probe trial of the MWM test. YC-1 treatment reversed the reduction of the “time spent in the escape platform’s quadrant” of 24-month-old rats. In the PA test, there was no significant difference in the 1st-day latency of rats in all groups. On the 2nd day, retention latency significantly decreased in the 24-month-old rats compared to 4-month-olds. YC-1 reversed the diminished retention latency in 24-month-old rats. YC-1 treatment and aging did not affect results of the locomotor activity test or the foot-shock sensitivity test, suggesting our results were not due to a change in motor activity or disability of the animals.ConclusionsOur findings suggest that activation of the NO-sGC-cGMP pathway plays an important role in spatial and emotional learning and memory functions in aged rats.

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“…Many studies have investigated TWAA and PA response in rats using NOS inhibitors and NO donors/precursors (Chien et al., 2008; Komsuoglu-Celikyurt et al., 2011; Kucukatay et al, 2009; Pitsikas et al, 2001; Utkan, Gocmez, Ozer, Gacar, & Aricioglu, 2012). Majority of these studies were carried out by administration of non-selective and putative partially selective NOS1 inhibitors and NO donors/precursors.…”

Section: Discussionmentioning

confidence: 99%

“…Molecular lines of evidence suggest that the NO system interacts extensively with glutaminergic and monoaminergic signaling pathways (Christopherson, Hillier, Lim, & Bredt, 1999; Duchemin, Neff, & Hadjiconstantinou, 2010; Kiss & Vizi, 2001; Kiss, Zsilla, & Vizi, 2004; Zabel et al, 2002). Experiments that pharmacologically manipulate NO signaling pathways also demonstrate the functional role of NO in learning and memory (Chien, Liang, & Fu, 2008; Komsuoglu-Celikyurt et al, 2011; Kucukatay, Hacioglu, Ozkaya, Agar, & Yargicoglu, 2009; Pitsikas et al, 2001). …”

Section: Introductionmentioning

confidence: 99%

Lack of neuronal nitric oxide synthase results in attention deficit hyperactivity disorder-like behaviors in mice.

Gao¹,

Heldt²

2015

Behavioral Neuroscience

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Nitric oxide (NO) is an important molecule for the proper development and function of the central nervous system. In this study, we investigated the behavioral alterations in the neuronal nitric oxide synthase knockout mice (NOS1 KO) with a deficient NO production mechanism in the brain, characterizing it as a potential rodent model for attention deficit / hyperactivity disorder (ADHD). NOS1 KO exhibited higher locomotor activity than their wildtype counterparts in a novel environment, as measured by open field (OF) test. In a two-way active avoidance paradigm (TWAA), we found sex-dependent effects, where male KO displayed deficits in avoidance and escape behavior, sustained higher incidences of shuttle crossings and higher incidences of inter-trial interval crossings, suggesting learning and/or performance impairments. On the other hand, female KO demonstrated few deficits in TWAA. Molsidomine (MSD), a NO donor, rescued TWAA deficits in male KO when acutely administered before training. In a passive avoidance paradigm, KO of both sexes displayed significantly shorter step-through latencies after training. Further, abnormal spontaneous motor activity rhythms were found in the KO during the dark phase of the day, indicating dysregulation of rhythmic activities. These data indicate that NOS1 KO mimic certain ADHD-like behaviors and could potentially serve as a novel rodent model for ADHD.

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Evidence for the involvement of neuronal nitric oxide synthase and soluble guanylate cyclase on cognitive functions in rats

Cited by 13 publications

References 45 publications

Effects of 7-NI and ODQ on memory in the passive avoidance, novel object recognition, and social transmission of food preference tests in mice

Effects of 7-NI and ODQ on memory in the passive avoidance, novel object recognition, and social transmission of food preference tests in mice

Effects of YC-1 on Learning and Memory Functions of Aged Rats

Lack of neuronal nitric oxide synthase results in attention deficit hyperactivity disorder-like behaviors in mice.

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