Antidepressant-like effect of 7-nitroindazole in the forced swimming test in rats

Yıldız, Fahrettin; Erden, Bekir Faruk; Ulak, Güner; Utkan, Tijen; Gacar, Nejat

doi:10.1007/s002139900316

Cited by 147 publications

(84 citation statements)

References 13 publications

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“…This notion is further supported by recent studies which have demonstrated that NOS inhibitors are as efficacious as antidepressants in reducing the duration of immobility in the mouse forced swimming test -a preclinical antidepressant screening procedure [4][5][6]. These anti-immobility effects are blocked by prior administration of the NO precursor, L-arginine [4,5].…”

Section: Introductionsupporting

confidence: 59%

Association Analysis for Neuronal Nitric Oxide Synthase Gene Polymorphism with Major Depression and Fluoxetine Response

Yu¹,

Chen

Wang

et al. 2003

Neuropsychobiology

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Nitric oxide (NO) is produced from its precursor L-arginine by the enzyme NO synthase (NOS), which includes at least three distinct isoforms – neuronal (nNOS), endothelial, and inducible NOS. Recent studies have implicated NOS in the mechanism that underlies the therapeutic efficacy of antidepressant medication. In addition, major depressive disorder (MDD) patients were found to have significantly higher plasma nitrate concentrations than normal subjects, an index of NO production, in comparison to normal subjects. In a population-based association study, we tested the hypothesis that the nNOS C276T polymorphism confers susceptibility to MDD. We also examined the association between this polymorphism and therapeutic fluoxetine response in 114 MDD patients who underwent a 4-week fluoxetine treatment. The results demonstrate that the nNOS variants are found at similar frequencies in MDD patients and healthy control subjects. Further, we did not discover any genetic variants that influenced the fluoxetine response in MDD patients treated with fluoxetine. Our findings suggest that this nNOS C276T polymorphism does not play a major role in the susceptibility to, or fluoxetine response in, MDD. However, the association between other NOS variants and MDD or antidepressant response, including sexual dysfunction, may warrant further investigation.

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Section: Introductionsupporting

confidence: 59%

Association Analysis for Neuronal Nitric Oxide Synthase Gene Polymorphism with Major Depression and Fluoxetine Response

Yu¹,

Chen

Wang

et al. 2003

Neuropsychobiology

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“…Accordingly, a rapidly increasing body of evidence coming from pharmacological studies in animals argues in favour of this hypothesis. [26][27][28][29][30][31][32][33][34][35] Finally, a landmark study by Akbarian et al, 36,37 followed by further histopathological investigations, 38 argues that nitrinergic neurons are pathologically altered in SCZ.…”

Section: Introductionmentioning

confidence: 99%

A neuronal nitric oxide synthase (NOS-I) haplotype associated with schizophrenia modifies prefrontal cortex function

et al. 2006

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Nitric oxide (NO) is a gaseous neurotransmitter thought to play important roles in several behavioral domains. On a neurobiological level, NO acts as the second messenger of the Nmethyl-D-aspartate receptor and interacts with both the dopaminergic as well as the serotonergic system. Thus, NO is a promising candidate molecule in the pathogenesis of endogenous psychoses and a potential target in their treatment. Furthermore, the chromosomal locus of the gene for the NO-producing enzyme NOS-I, 12q24.2, represents a major linkage hot spot for schizophrenic and bipolar disorder. To investigate whether the gene encoding NOS-I (NOS1) conveys to the genetic risk for those diseases, five NOS1 polymorphisms as well as a NOS1 mini-haplotype, consisting of two functional polymorphisms located in the transcriptional control region of NOS1, were examined in 195 chronic schizophrenic, 72 bipolar-I patients and 286 controls. Single-marker association analysis showed that the exon 1c promoter polymorphism was linked to schizophrenia (SCZ), whereas synonymous coding region polymorphisms were not associated with disease. Long promoter alleles of the repeat polymorphism were associated with less severe psychopathology. Analysis of the mini-haplotype also revealed a significant association with SCZ. Mutational screening did not detect novel exonic polymorphisms in patients, suggesting that regulatory rather than coding variants convey the genetic risk on psychosis. Finally, promoter polymorphisms impacted on prefrontal functioning as assessed by neuropsychological testing and electrophysiological parameters elicited by a Go-Nogo paradigm in 48 patients (continuous performance test). Collectively these findings suggest that regulatory polymorphisms of NOS1 contribute to the genetic risk for SCZ, and modulate prefrontal brain functioning.

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“…Drug doses were selected according to behavioral and neurochemical studies showing the drugs to have the intended effect [23,25] . 7-NI and L -arginine, at the doses used in this study, were previously shown to have no effect on locomotor activity [3,4,16] . Since it was reported that maximal inhibition of NOS by 7-NI occurs at 30 min after intraperitoneal injection [24,25] , 7-NI (2.5, 5, 10 mg/kg), L -arginine (200 mg/kg) or vehicle was administered intraperitoneally 30 min prior to the three-panel runway task, which was performed when the animals fulfilled the learning criteria.…”

Section: Drugs and Treatmentsmentioning

confidence: 99%

“…NO was implicated in the regulation of various behavioral, cognitive and emotional processes such as aggression, anxiety, depression and locomotion [2][3][4] . It has recently been suggested to play a role in modulating learning and memory [5] .…”

Section: Introductionmentioning

confidence: 99%

Effects of <i>L</i>-Arginine on 7-Nitroindazole-Induced Reference and Working Memory Performance of Rats

et al. 2009

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Background/Aims: This study was performed in order to elucidate the effects of 7-nitroindazole (7-NI) and L-arginine on cognitive functions of rats in a three-panel runway task. Methods: 7-NI (2.5, 5, 10 mg/kg) and L-arginine (200 mg/kg) were injected intraperitoneally into male Wistar rats 30 min before the test. Results: 7-NI (5, 10 mg/kg) significantly increased the number of errors (pushes made on the 2 incorrect panels of the panel gate at 4 choice points) and prolonged the latency of reference memory in the three-panel runway task. The negative effects of 7-NI on reference memory was counteracted by L-arginine, a substrate for nitric oxide synthase. While having no effect on the number of working memory errors in working memory trials, 7-NI prolonged the latency from the 2nd to the 6th trial at the 5- and 10-mg/kg doses. Concurrent administration with L-arginine counteracted the 7-NI-induced prolongation of latency from the 2nd to the 6th trial. Conclusion: 7-NI impaired reference memory but not working memory in the three-panel runway test. Moreover, nitric oxide played an essential role in the development of reference memory and the negative effects of 7-NI on memory were counteracted by L-arginine.

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Antidepressant-like effect of 7-nitroindazole in the forced swimming test in rats

Abstract: Our findings suggest that NO might be an important modulator of depression in rats.

Cited by 147 publications

References 13 publications

Association Analysis for Neuronal Nitric Oxide Synthase Gene Polymorphism with Major Depression and Fluoxetine Response

Association Analysis for Neuronal Nitric Oxide Synthase Gene Polymorphism with Major Depression and Fluoxetine Response

A neuronal nitric oxide synthase (NOS-I) haplotype associated with schizophrenia modifies prefrontal cortex function

Effects of <i>L</i>-Arginine on 7-Nitroindazole-Induced Reference and Working Memory Performance of Rats

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