Chronic treatment with mood stabilizer lithium inhibits amphetamine-induced risk-taking manic-like behaviors

Zhu, Zhou; Wang, Ying; Tan, Hua; Bharti, Veni; Che, Yi; Wang, Junfeng

doi:10.1016/j.neulet.2015.07.027

Cited by 15 publications

(10 citation statements)

References 36 publications

(52 reference statements)

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“…Several lines of evidence had also demonstrated that chronic administration of amph could induce a wide range of manic‐like behaviour in rodents, being considered a suitable animal model (Minassian et al., 2016). Herein, the treatment with HDAC inhibitors, VPA and SB, were able to decrease this d‐amph‐induced hyperactivity in the animals, as described in previous studies (Resende et al., 2013; Zhou et al., 2015).…”

Section: Discussionsupporting

confidence: 72%

Role of epigenetic regulatory enzymes in animal models of mania induced by amphetamine and paradoxical sleep deprivation

Varela

Resende²,

Dal‐Pont³

et al. 2020

Eur J of Neuroscience

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It is known that bipolar disorder has a multifactorial aetiology where the interaction between genetic and environmental factors is responsible for its development. Because of this, epigenetics has been largely studied in psychiatric disorders. The present study aims to evaluate the effects of histone deacetylase inhibitors on epigenetic enzyme alterations in rats or mice submitted to animal models of mania induced by dextro‐amphetamine or sleep deprivation, respectively. Adult male Wistar rats were subjected to 14 days of dextro‐amphetamine administration, and from the eighth to the fourteenth day, the animals were treated with valproate and sodium butyrate in addition to dextro‐amphetamine injections. Adult C57BL/6 mice received 7 days of valproate or sodium butyrate administration, being sleep deprived at the last 36 hr of the protocol. Locomotor and exploratory activities of rats and mice were evaluated in the open‐field test, and histone deacetylase, DNA methyltransferase, and histone acetyltransferase activities were assessed in the frontal cortex, hippocampus, and striatum. Dextro‐amphetamine and sleep deprivation induced hyperactivity and increased histone deacetylase and DNA methyltransferase activities in the animal's brain. Valproate and sodium butyrate were able to reverse hyperlocomotion induced by both animal models, as well as the alterations on histone deacetylase and DNA methyltransferase activities. There was a positive correlation between enzyme activities and number of crossings for both models. Histone deacetylase and DNA methyltransferase activities also presented a positive correlation between theirselves. These results suggest that epigenetics can play an important role in BD pathophysiology as well as in its treatment.

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Section: Discussionsupporting

confidence: 72%

Role of epigenetic regulatory enzymes in animal models of mania induced by amphetamine and paradoxical sleep deprivation

Varela

Resende²,

Dal‐Pont³

et al. 2020

Eur J of Neuroscience

View full text Add to dashboard Cite

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“…Such a shift in this balance has also been interpreted as a result of increased motivation for risk (Labonte et al, 2012; Hodgson et al, 2008), which may result from impaired risk-based decision making. Previous work has shown that repeated drug exposure in adult rats will also increase risk-taking behavior in other tasks (Zhou et al, 2015). Dopamine signaling in the mPFC has previously been shown to mediate decision making, including risk-based decisions (St Onge and Floresco, 2010; Simon et al, 2011), and it is noteworthy that temporary inactivation of the mPFC by local infusion of muscimol increases open arm activity (Shah et al, 2004; Solati et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Timing of amphetamine exposure in relation to puberty onset determines its effects on anhedonia, exploratory behavior, and dopamine D1 receptor expression in young adulthood

Kang

Galvez

et al. 2016

Neuroscience

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Non-medical use of amphetamine (AMPH) among adolescents is prevalent, which is problematic given the potential consequences of developmental drug exposure on brain function and behavior. Previously we found in adult male rats that AMPH exposure starting before puberty induces a persistent decrease in dopamine D1 receptor (D1R) function in the medial prefrontal cortex (mPFC). Here we investigated if this dysfunction was associated with changes in D1R expression in the mPFC and nucleus accumbens (NAc). We also determined if starting drug exposure well before or near the onset of puberty would influence AMPH-induced changes in D1R expression and behavior. Male and female Sprague-Dawley rats were treated once every other day (10 injections total) with saline or 3 mg/kg AMPH (i.p.) from either postnatal day (P) 27 to 45 (pre-puberty groups; pre-P) or P37 to 55 (peri-puberty groups; peri-P). After 1, 7 and 21 days of withdrawal, sucrose preference tests were performed to assess anhedonia. Exploratory behavior was studied in an open-field arena and on an elevated plus maze (EPM). Rats were then sacrificed for western blot analysis of D1R expression. We found that AMPH withdrawal induced decreases in sucrose preference that persisted in rats with peri-P onset treatment. Pre-P onset AMPH exposure led to increased open arm exploration in the EPM test, as well as a decreased D1R level in the mPFC but not NAc. Our results demonstrated that AMPH exposure starting at different developmental stages resulted in distinct neurobehavioral abnormalities, suggesting an important role of exposure timing in drug-induced plasticity.

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“…Previous preclinical studies showed that lithium reversed hyperactivity and risktaking behavior after repeated injections of amphetamine [107,108], and thus was considered a validated model of mania in rats [109][110][111]. Therefore, studies using this model of mania confirmed that lithium prevented the amphetamine-induced inhibition of ETC complexes I, II, III, and IV in the hippocampus, striatum and prefrontal cortex.…”

Section: Lithium Influences Inflammation and Energy Metabolismmentioning

confidence: 83%

Inflammation-Related Changes in Mood Disorders and the Immunomodulatory Role of Lithium

Sakrajda

Szczepankiewicz

2021

IJMS

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Mood disorders are chronic, recurrent diseases characterized by changes in mood and emotions. The most common are major depressive disorder (MDD) and bipolar disorder (BD). Molecular biology studies have indicated an involvement of the immune system in the pathogenesis of mood disorders, and showed their correlation with altered levels of inflammatory markers and energy metabolism. Previous reports, including meta-analyses, also suggested the role of microglia activation in the M1 polarized macrophages, reflecting the pro-inflammatory phenotype. Lithium is an effective mood stabilizer used to treat both manic and depressive episodes in bipolar disorder, and as an augmentation of the antidepressant treatment of depression with a multidimensional mode of action. This review aims to summarize the molecular studies regarding inflammation, microglia activation and energy metabolism changes in mood disorders. We also aimed to outline the impact of lithium on these changes and discuss its immunomodulatory effect in mood disorders.

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Chronic treatment with mood stabilizer lithium inhibits amphetamine-induced risk-taking manic-like behaviors

Cited by 15 publications

References 36 publications

Role of epigenetic regulatory enzymes in animal models of mania induced by amphetamine and paradoxical sleep deprivation

Role of epigenetic regulatory enzymes in animal models of mania induced by amphetamine and paradoxical sleep deprivation

Timing of amphetamine exposure in relation to puberty onset determines its effects on anhedonia, exploratory behavior, and dopamine D1 receptor expression in young adulthood

Inflammation-Related Changes in Mood Disorders and the Immunomodulatory Role of Lithium

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