Neurochemistry of the Nucleus Accumbens and its Relevance to Depression and Antidepressant Action in Rodents

Shirayama, Yukihiko; Chaki, Shigeyuki

doi:10.2174/157015906778520773

Cited by 190 publications

(122 citation statements)

References 167 publications

(229 reference statements)

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“…: Rogge et al, 2008;Shirayama and Chaki, 2006). More specifically, in a Korean population, association was found between a polymorphism in intron 1 of the CART gene and alcoholism (Jung et al, 2004), and CART-peptide containing neurons are activated by acute administration of psychostimulants (Rogge et al, 2008;Shirayama and Chaki, 2006). Sex-specificity has been consistently found in stress adaptation and stress-induced brain diseases (Afifi, 2007;Kessler et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…There is substantial evidence connecting CART with reward circuitries in the mammalian brain (for review see e.g. : Rogge et al, 2008;Shirayama and Chaki, 2006). More specifically, in a Korean population, association was found between a polymorphism in intron 1 of the CART gene and alcoholism (Jung et al, 2004), and CART-peptide containing neurons are activated by acute administration of psychostimulants (Rogge et al, 2008;Shirayama and Chaki, 2006).…”

Section: Discussionmentioning

confidence: 99%

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Sex-specific differences in the dynamics of cocaine- and amphetamine-regulated transcript and nesfatin-1 expressions in the midbrain of depressed suicide victims vs. controls

Bloem

Morava

et al. 2012

Neuropharmacology

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a b s t r a c tAn intriguing novel pathophysiological insight into mood disorders is the notion that one's metabolic status influences mood. In rodents, cocaine-and amphetamine-regulated transcript (CART) and nesfatin-1/NUCB2 have not only been implicated in metabolism, but in the pathobiology of anxiety and depressive-like behaviour, however they have not previously been investigated in depressed subjects. Both peptides are highly expressed in centrally projecting neurons in the Edinger-Westphal nucleus (EWcp) in the midbrain. The EWcp has been implicated in stress adaptation and stress-related mood disorders like major depressive disorder in a sex-specific manner. This is intriguing, given the fact that females have higher prevalence of mood disorders. Here, we hypothesized that the expression of CART and nesfatin-1 in EWcp would exhibit a sex-specific difference between depressed suicide victims vs. controls. We found that CART and nesfatin/NUCB2 colocalized in the human EWcp, and that CART mRNA content was much higher in both male (Â3.8) and female (Â5.9) drug-free suicide victims than in controls (persons who died without any diagnosed neurodegenerative or psychiatric disorder). Similarly, NUCB2 mRNA content was also higher (Â1.8) in male suicides, whereas in female suicide victims, these contents were Â2.7 lower compared to controls. These observations are the first to show changes in the dynamics of CART and nesfatin/NUCB2 expressions in the midbrain of drug-free depressed suicide victims vs. controls.This article is part of a Special Issue entitled 'Anxiety and Depression'.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Sex-specific differences in the dynamics of cocaine- and amphetamine-regulated transcript and nesfatin-1 expressions in the midbrain of depressed suicide victims vs. controls

Bloem

Morava

et al. 2012

Neuropharmacology

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“…However, these medicines actually have no antidepressant effect. 44) To avoid false positives in the following test, normal mice were exposed to the open-field apparatus for 5 min. The results showed that AST did not increase or reduce locomotor activity of normal mice, indicating that AST does not produce neural excitability.…”

Section: Discussionmentioning

confidence: 99%

Antidepressant Activity of Astilbin: Involvement of Monoaminergic Neurotransmitters and BDNF Signal Pathway

Guo

et al. 2014

Biological & Pharmaceutical Bulletin

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Depression and related mood disorders are among the world's greatest public health problems. Previous studies have demonstrated that astilbin (AST) has broad pharmacological functions which may modulate numerous pathways, such as antioxidant, scavenging free radicals, anti-inflammatory and so on, similarly to some of other flavonoids. In this study, the antidepressant-like effect of AST was investigated using chronic unpredictable mild stress ( Key words depression; astilbin; chronic unpredictable mild stress; serotonin; dopamine; brain-derived neurotrophic factor Depression is a serious medical illness that characterized by affective disorder. According to the World Health Organization (WHO), by the year 2030, depression will result in more years of life lost to disability than any other illness.1) At present, most antidepressants used clinically with low efficacy and many side effects can not meet the clinical needs. Therefore, with the increased prevalence of depression and social burden every year, the development of new antidepressants is becoming a top priority.Despite the fact that the molecular and cellular mechanisms remain unclear, a leading hypothesis of depression recently suggests that neurotrophic factors and adult neurogenesis play critical roles in mediating the behavioural responses to antidepressants.2) The brain-derived neurotrophic factor (BDNF) is closely related to neuronal survival and neurogenesis and plays an important role in animal models of depression. Various stress procedures including chronic unpredictable mild stress (CUMS) result in obviously decreases of BDNF expression in the brain, while chronic administration of almost all kinds of antidepressants including imipramine regulates BDNF levels. [3][4][5] The extracellular signal-regulated kinases (ERK) and AKT pathways are the two important downstream signaling pathways of BDNF. It has been reported that some of new antidepressants under development upregulate the expression of BDNF in different brain regions of stress mice via promoting the phosphorylation of ERK1/2 and AKT and thus activating the ERK, AKT pathways to produce antidepressant effects. [6][7][8] In recent studies, natural flavonoids especially resveratrol, tea polyphenols and curcumin show attractive prospect in the field of neural protection research.7,9,10) There is growing evidence indicated that flavonoids ameliorate the symptoms of depression via upregulating the levels of monoaminergic neurotransmitters 11) and promoting the expression of neurotrophic factors. 12,13)

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“…Chronic smoking has been shown to inhibit MAO (monoamine oxidase) enzyme, thus producing antidepressive effects. 1,2 Nicotine patches can improve the mood in depressed patients. 3 However, it is unclear, if nicotine or other chemicals directly affect the brain of a depressed person.…”

Section: Introductionmentioning

confidence: 99%

Effect of nicotine on serotonin (5-HT) levels in brain of depressed rats

Bhalsinge

Barde

Worlikar

et al. 2017

Int J Basic Clin Pharmacol

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Background: Reduction in brain serotonin (5-HT) levels contributes to depression. Nicotine may have antidepressant properties and smokers self-medicate underlying depression. Epidemiological findings suggest that smokers more often demonstrate depressive symptoms than non-smokers and depressed patients are less likely to cease smoking. Therefore, the study was planned to evaluate the effect of nicotine on serotonin levels in brain of depressed rats.Methods: Antidepressant action of study drugs was evaluated using isolation induced hyperactivity model in rats. Rats were divided into five groups with six rats in each group. Study groups: Vehicle in normal rats 1 ml/kg (subcutaneous); vehicle after isolation 1ml/kg (subcutaneous); imipramine 10 mg/kg (intraperitoneal) for 7 consecutive days; single dose of nicotine 0.4 mg/kg (subcutaneous); single dose of nicotine 0.2 mg/kg (inhalational). Brain serotonin assay was carried out. The statistical significance was determined by ANOVA followed by Tukey test (p<0.05).Results: Serotonin levels (55.93ng/g of brain tissue) in rats after isolation were significantly less than in normal rats (335.87ng/g) (p<0.001). In imipramine treated group, serotonin levels (301.4ng/g) after isolation were highly significant as compared to serotonin levels in vehicle treated group after isolation (p<0.001). Nicotine administered by subcutaneous and inhalational route showed significantly higher brain serotonin levels, i.e. 175ng/g and 254.62ng/g respectively as compared to vehicle treated rats after isolation (p<0.001).Conclusions: Single dose nicotine (inhalational) produced significant antidepressant action comparable to that of seven days’ treatment of standard antidepressant drug imipramine in rats. In rats, nicotine by both routes i.e. subcutaneous and inhalational increased serotonergic activity.

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Neurochemistry of the Nucleus Accumbens and its Relevance to Depression and Antidepressant Action in Rodents

Cited by 190 publications

References 167 publications

Sex-specific differences in the dynamics of cocaine- and amphetamine-regulated transcript and nesfatin-1 expressions in the midbrain of depressed suicide victims vs. controls

Sex-specific differences in the dynamics of cocaine- and amphetamine-regulated transcript and nesfatin-1 expressions in the midbrain of depressed suicide victims vs. controls

Antidepressant Activity of Astilbin: Involvement of Monoaminergic Neurotransmitters and BDNF Signal Pathway

Effect of nicotine on serotonin (5-HT) levels in brain of depressed rats

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