Citalopram decreases tryptophan 2,3-dioxygenase activity and brain 5-HT turnover in swim stressed rats

Ara, Iffat; Bano, Sarnina

doi:10.1016/s1734-1140(12)70851-4

Cited by 36 publications

(33 citation statements)

References 35 publications

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“…It has been demonstrated that a subchronic treatment of the racemic mixture citalopram (20 mg/kg) in mice was effective in the forced swimming test, without affecting locomotor activity in open field [49,50]. Similar to our results, repeated exposure to citalopram did not alter locomotor activity but selectively affected anxiety-related behavioural indices in the FSL rats, model of depression [51].…”

Section: Discussionsupporting

confidence: 88%

Behavioural and transcriptional effects of escitalopram in the chronic escape deficit model of depression

Benatti

Alboni

Blom

et al. 2014

Behavioural Brain Research

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Section: Discussionsupporting

confidence: 88%

Behavioural and transcriptional effects of escitalopram in the chronic escape deficit model of depression

Benatti

Alboni

Blom

et al. 2014

Behavioural Brain Research

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“…The antidepressant citalopram exerted antidepressive-like effects and increased turnover of 5-HT via IDO inhibition in the hippocampus, amygdala and hypothalamus of stressed rats (Ara and Bano, 2012). Fluoxetine administration reduced depressive-like behaviors in tumor-bearing mice, but did not have an effect on KMO mRNA or IDO expression (Norden et al, 2015).…”

Section: Resultsmentioning

confidence: 99%

Kynurenine pathway dysfunction in the pathophysiology and treatment of depression: Evidences from animal and human studies

Réus¹,

Jansen

Titus³

et al. 2015

Journal of Psychiatric Research

197

113

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Treatment-resistant depression affects up to 20% of individuals suffering from major depressive disorder (MDD). The medications currently available to treat depression, including serotonin re-uptake inhibitors (SSRIs), monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants (TCAs), fail to produce adequate remission of depressive symptoms for a large number of patients. The monoamine hypothesis upon which these medications are predicated should be expanded and revised as research elucidates alternative mechanisms of depression and effective methods to treat the underlying pathologic consequences. Research into the role of tryptophan degradation and the kynurenine pathway in the setting of inflammation has brought new insight into potential etiologies of MDD. Further investigation into the connection between inflammatory mediators, tryptophan degradation, and MDD can provide many targets for novel antidepressant therapies. Thus, this review will highlight the role of the kynurenine pathway in the pathophysiology of depression, as well as a novel therapeutic target to classic and new modulators to treat depression based on findings from preclinical and clinical studies.

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“…In general, stressors like acute restraint, acute novelty, and repeated swim stress enhanced serotonin turnover in prefrontal-limbic and associated areas of various rat and mouse strains (Ara and Bano, 2012; Browne et al, 2011; Drossopoulou et al, 2004; Miura et al, 2002). Following acute swim stress in the FSTv, serotonin turnover was elevated in the hypothalamus of H-FSS mice (this study) and in the amygdala and prefrontal cortex, but not hypothalamus, of Sprague Dawley rats (Connor et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Effect of acute swim stress on plasma corticosterone and brain monoamine levels in bidirectionally selected DxH recombinant inbred mouse strains differing in fear recall and extinction

Browne

Hanke

Rose

et al. 2014

Stress

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Stress-induced changes in plasma corticosterone and central monoamine levels were examined in mouse strains that differ in fear-related behaviors. Two DxH recombinant inbred mouse strains with a DBA/2J background, which were originally bred for a high (H-FSS) and low fear-sensitized acoustic startle reflex (L-FSS), were used. Levels of noradrenaline, dopamine, and serotonin and their metabolites (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA) were studied in the amygdala, hippocampus, medial prefrontal cortex, striatum, hypothalamus, and brainstem. H-FSS mice exhibited increased fear levels and a deficit in fear extinction (within-session) in the auditory fear-conditioning test, and depressive-like behavior in the acute forced swim stress test. They had higher tissue noradrenaline and serotonin levels and lower dopamine and serotonin turnover under basal conditions, although they were largely insensitive to stress-induced changes in neurotransmitter metabolism. In contrast, acute swim stress increased monoamine levels but decreased turnover in the less fearful L-FSS mice. L-FSS mice also showed a trend toward higher basal and stress-induced corticosterone levels and an increase in noradrenaline and serotonin in the hypothalamus and brainstem 30 minutes after stress compared to H-FSS mice. Moreover, the dopaminergic system was activated differentially in the medial prefrontal cortex and striatum of the two strains by acute stress. Thus, H-FSS mice showed increased basal noradrenaline tissue levels compatible with a fear phenotype or chronic stressed condition. Low corticosterone levels and the poor monoamine response to stress in H-FSS mice may point to mechanisms similar to those found in principal fear disorders or posttraumatic stress disorder.

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Citalopram decreases tryptophan 2,3-dioxygenase activity and brain 5-HT turnover in swim stressed rats

Cited by 36 publications

References 35 publications

Behavioural and transcriptional effects of escitalopram in the chronic escape deficit model of depression

Behavioural and transcriptional effects of escitalopram in the chronic escape deficit model of depression

Kynurenine pathway dysfunction in the pathophysiology and treatment of depression: Evidences from animal and human studies

Effect of acute swim stress on plasma corticosterone and brain monoamine levels in bidirectionally selected DxH recombinant inbred mouse strains differing in fear recall and extinction

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