Reduction in endogenous cardiac steroids protects the brain from oxidative stress in a mouse model of mania induced by amphetamine

Hodes, Anastasia; Lifschytz, Tzuri; Rosen, Haim; Ben-Ami, Hagit Cohen; Lichtstein, David

doi:10.1016/j.brainresbull.2018.01.016

Cited by 17 publications

(12 citation statements)

References 58 publications

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“…In the same direction, Amph detrimental effects (regarding ROS, inflammatory cytokines and dopaminergic degeneration) were described in limbic areas, whereas they were not detected in HPC (Belcher, O'Dell, & Marshall, ; Dietrich et al, ; Jiang et al, ; Tan et al, ; Valvassori et al, ). On the contrary, vascular, glial, and oxidative markers increase have been described in HPC after higher doses of Amph or a very short time after the last administration (i.e., after 24 hr), suggesting time‐ and dose‐dependent alterations (Che et al, ; Hodes, Lifschytz, Rosen, Cohen Ben‐Ami, & Lichtstein, ; de Souza et al, ). Since the main long‐lasting effect of Amph exposure is DA neurotransmission imbalance, PFC regional susceptibility could be triggered by its greater dopaminergic innervation (Sofuoglu, ).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II modulates amphetamine‐induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine

Marchese

Occhieppo

Basmadjian

et al. 2019

Eur J of Neuroscience

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Amphetamine‐induced neuroadaptations involve vascular damage, neuroinflammation, a hypo‐functioning prefrontal cortex (PFC), and cognitive alterations. Brain angiotensin II, through angiotensin type 1 receptor (AT1‐R), mediates oxidative/inflammatory responses, promoting endothelial dysfunction, neuronal oxidative damage and glial reactivity. The present work aims to unmask the role of AT1‐R in the development of amphetamine‐induced changes over glial and vascular components within PFC and hippocampus. Attention deficit was evaluated as a behavioral neuroadaptation induced by amphetamine. Brain microvessels were isolated to further evaluate vascular alterations after amphetamine exposure. Male Wistar rats were administered with AT1‐R antagonist, candesartan, followed by repeated amphetamine. After one week drug‐off period, animals received a saline or amphetamine challenge and were evaluated in behavioral tests. Afterward, their brains were processed for cresyl violet staining, CD11b (microglia marker), GFAP (astrocyte marker) or von Willebrand factor (vascular marker) immunohistochemistry, and oxidative/cellular stress determinations in brain microvessels. Statistical analysis was performed by using factorial ANOVA followed by Bonferroni or Tukey tests. Repeated amphetamine administration increased astroglial and microglial markers immunoreactivity, increased apoptotic cells, and promoted vascular network rearrangement at the PFC concomitantly with an attention deficit. Although the amphetamine challenge improved the attentional performance, it triggers detrimental effects probably because of the exacerbated malondialdehyde levels and increased heat shock protein 70 expression in microvessels. All observed amphetamine‐induced alterations were prevented by the AT1‐R blockade. Our results support the AT1‐R involvement in the development of oxidative/inflammatory conditions triggered by amphetamine exposure, affecting cortical areas and increasing vascular susceptibility to future challenges.

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Section: Discussionmentioning

confidence: 99%

Angiotensin II modulates amphetamine‐induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine

Marchese

Occhieppo

Basmadjian

et al. 2019

Eur J of Neuroscience

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“…The relation between the central and peripheral RAASes with central and peripheral EO is still not completely understood [ 55 ], but it was discovered that EO-induced signaling in neurons had positive and direct consequences on rat brain in terms of brain cells survival [ 57 ]. Similarly, in mouse models, the reduction of endogenous steroids seems to have a protective effect on oxidative stress for CNS [ 58 ]. Endogenous steroids, in particular EO-like compounds, were also described as potential risk factors involved in the etiology of bipolar disorder [ 59 ], mania [ 60 ] and depression [ 61 ].…”

Section: The Correlation Between Endogenous Ouabain and Organ Damamentioning

confidence: 99%

Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases

Simonini

Casanova

Citterio

et al. 2018

IJMS

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The endogenous ouabain (EO) is a steroid hormone secreted by the adrenal gland with cardio-tonic effects. In this article, we have reviewed and summarized the most recent reports about EO, particularly with regard to how it may interact with specific genetic backgrounds. We have focused our attention on the EO’s potential pathogenic role in several diseases, including renal failure, essential hypertension and heart failure. Notably, these reports have demonstrated that EO acts as a pro-hypertrophic and growth-promoting hormone, which might lead to a cardiac remodeling affecting cardiovascular functions and structures. In addition, a possible role of EO in the development of acute kidney injury has been hypothesized. During the last decays, many important improvements permitted a deeper understanding of EO’s metabolisms and functions, including the characteristics of its receptor and the effects of its activation. Such progresses indicated that EO has significant implications in the pathogenesis of many common diseases. The patho-physiological role of EO in the development of hypertension and other cardiac and renal complications have laid the basis for the development of a new selective compound that could selectively modulate the genetic and molecular mechanisms involved in EO’s action. It is evident that the knowledge of EO has incredibly increased; however, many important areas remain to be further investigated.

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“…The Na + , K + -ATPase-ECS interaction leads to changes in the membrane electrical potential, and the activation of mitogen-activated protein kinase (ERK, or MAPK), protein kinase B (AKT), and nuclear factor kappa-light-chain-enhancer (NFκB) [19,71], which modifies neuronal activity and neurotransmission that, in turn, participate in the regulation of behavior and BD. The oxidative stress and inflammation, which are also involved in the Na + , K + -ATPase-ECS interaction [6,29], may add to the compromised brain biochemistry and support the vicious circle of depression in BD. We also suggest that the levels of ECS are changed in the mania stage, which may cause the compromised interaction of ECS and Na + , K + -ATPase.…”

Section: Discussionmentioning

confidence: 99%

“…A reduction in brain ECS had a protective effect in depressive-like behavior in rats [26], with concomitant alterations in catecholamine levels in specific brain regions [28]. Furthermore, a reduction in brain ECS also protected against manic-like behavior induced by amphetamine (AMPH) in mice [27], an effect that is associated with protection of the brain from oxidative stress [29].…”

Section: Of 16mentioning

confidence: 99%

Na+, K+-ATPase α Isoforms and Endogenous Cardiac Steroids in Prefrontal Cortex of Bipolar Patients and Controls

Singh¹,

Федорова

Wei

et al. 2020

IJMS

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Bipolar disorder is a chronic multifactorial psychiatric illness that affects the mood, cognition, and functioning of about 1–2% of the world’s population. Its biological basis is unknown, and its treatment is unsatisfactory. The α1, α2, and α3 isoforms of the Na+, K+-ATPase, an essential membrane transporter, are vital for neuronal and glial function. The enzyme and its regulators, endogenous cardiac steroids like ouabain and marinobufagenin, are implicated in neuropsychiatric disorders, bipolar disorder in particular. Here, we address the hypothesis that the α isoforms of the Na+, K+-ATPase and its regulators are altered in the prefrontal cortex of bipolar disease patients. The α isoforms were determined by Western blot and ouabain and marinobufagenin by specific and sensitive immunoassays. We found that the α2 and α3 isoforms were significantly higher and marinobufagenin levels were significantly lower in the prefrontal cortex of the bipolar disease patients compared with those in the control. A positive correlation was found between the levels of the three α isoforms in all samples and between the α1 isoform and ouabain levels in the controls. These results are in accordance with the notion that the Na+, K+-ATPase-endogenous cardiac steroids system is involved in bipolar disease and suggest that it may be used as a target for drug development.

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Reduction in endogenous cardiac steroids protects the brain from oxidative stress in a mouse model of mania induced by amphetamine

Cited by 17 publications

References 58 publications

Angiotensin II modulates amphetamine‐induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine

Angiotensin II modulates amphetamine‐induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine

Endogenous Ouabain and Related Genes in the Translation from Hypertension to Renal Diseases

Na+, K+-ATPase α Isoforms and Endogenous Cardiac Steroids in Prefrontal Cortex of Bipolar Patients and Controls

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