Atomoxetine, a selective norepinephrine reuptake inhibitor, improves short‐term histological outcomes after hypoxic‐ischemic brain injury in the neonatal male rat

Toshimitsu, Masatake; Kamei, Yoshimasa; Ichinose, Mari; Seyama, Takahiro; Imada, Shinya; Iriyama, Takayuki; Fujii, Tomoyuki

doi:10.1016/j.ijdevneu.2018.03.011

Cited by 8 publications

(6 citation statements)

References 75 publications

(115 reference statements)

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“…Microglia provide trophic support to neurons and endothelial cells, notably by producing BDNF, IGF-1/2 and TGF-ß such that disrupted growth factor production in microglia could interrupt cortical layer formation (Ueno et al, 2013 ). Microglial cells are inflammatory phenotypes initially associated with brain injury (Toshimitsu et al, 2018 ). After ischemic injury to the striatum, microglial cells displayed an M2 phenotype.…”

Section: Microglia and Neurogenesismentioning

confidence: 99%

Switching of the Microglial Activation Phenotype Is a Possible Treatment for Depression Disorder

Zhang

You

2018

Front. Cell. Neurosci.

229

158

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Major depressive disorder (MDD) is a common emotional cognitive disorder that seriously affects people’s physical and mental health and their quality of life. Due to its clinical and etiological heterogeneity, the molecular mechanisms underpinning MDD are complex and they are not fully understood. In addition, the effects of traditional drug therapy are not ideal. However, postmortem and animal studies have shown that overactivated microglia can inhibit neurogenesis in the hippocampus and induce depressive-like behaviors. Nonetheless, the molecular mechanisms by which microglia regulate nerve regeneration and determine depressive-like behaviors remain unclear. As the immune cells of the central nervous system (CNS), microglia could influence neurogenesis through the M1 and M2 subtypes, and these may promote depressive-like behaviors. Microglia may be divided into four main states or phenotypes. Under stress, microglial cells are induced into the M1 type, releasing inflammatory factors and causing neuroinflammatory responses. After the inflammation fades away, microglia shift into the alternative activated M2 phenotypes that play a role in neuroprotection. These activated M2 subtypes consist of M2a, M2b and M2c and their functions are different in the CNS. In this article, we mainly introduce the relationship between microglia and MDD. Importantly, this article elucidates a plausible mechanism by which microglia regulate inflammation and neurogenesis in ameliorating MDD. This could provide a reliable basis for the treatment of MDD in the future.

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Section: Microglia and Neurogenesismentioning

confidence: 99%

Switching of the Microglial Activation Phenotype Is a Possible Treatment for Depression Disorder

Zhang

You

2018

Front. Cell. Neurosci.

229

158

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“…Primary mesencephalic cultures treated chronically with NE have a significantly reduced rate of cell death, increased neuritic processes, and reduced production of reactive oxygen species when compared to untreated cultures, and this phenotype resembles cultures treated with traditional antioxidants ( Troadec et al, 2001 , 2002 ). Increasing synaptic NE was shown to be protective against neuron loss and inflammation in a model of hypoxic-ischemia ( Toshimitsu et al, 2018 ). While NE ligation of ARs directly facilitates neuroprotection by several mechanisms, the neuroprotective effects are not always blocked by AR antagonists, suggesting NE-mediated protection may also occur indirectly.…”

Section: Neuroprotective Effectsmentioning

confidence: 99%

α-Synuclein and Noradrenergic Modulation of Immune Cells in Parkinson’s Disease Pathogenesis

2018

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α-synuclein (α-syn) pathology and loss of noradrenergic neurons in the locus coeruleus (LC) are among the most ubiquitous features of Parkinson’s disease (PD). While noradrenergic dysfunction is associated with non-motor symptoms of PD, preclinical research suggests that the loss of LC norepinephrine (NE), and subsequently its immune modulatory and neuroprotective actions, may exacerbate or even accelerate disease progression. In this review, we discuss the mechanisms by which α-syn pathology and loss of central NE may directly impact brain health by interrupting neurotrophic factor signaling, exacerbating neuroinflammation, and altering regulation of innate and adaptive immune cells.

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“…As duloxetine, pre or post treatment with atomoxetine, a selective norepinephrine reuptake inhibitor, attenuated glial activation in ischemic CA1 region after transient ischemia and improved neuronal outcomes after hypoxic ischemia [65]. Atomoxetine overexpressed BDNF that upregulates several antioxidant enzymes and exerts antiapoptotic activity [66]. These results indicated that enhancement of both serotonin and norepinephrine signaling in brain could be a potential effective therapeutic strategy for cerebral ischemia treatment.…”

Section: The Role Of Seretonin Norepinephrine Reuptake Inhibitors (Snris) and Other Antidepressants On Cerebral Ischemiamentioning

confidence: 87%

“…Atomoxetine, duloxetine and venlafaxine upregulate the expression of several antioxidant enzymes as catalase and superoxide dismutase. Atomoxetine also overexpresses BDNF that attenuates neuronal damage and enhances cell survival [65,66,68]. All these previous mechanisms explained the neuroprotective role of different SSRIs in experimental cerebral ischemia induced by different animal models.…”

Section: Proposed Mechanisms Of the Neuroprotective Role Of Ssris And Snris In Cerebral Ischemiamentioning

confidence: 91%

Therapeutic potential of serotonin in ischemic stroke

El-hameed

Baket

El‐Daly

et al. 2021

Journal of advanced Biomedical and Pharmaceutical Sciences

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Stroke is a leading cause of death and neurological disability worldwide. Survivors of ischemic stroke usually suffer from impairment in motor function, visual field defect, speech disorders and depression. Cerebral levels of several neurotransmitters such as dopamine, 5-hydroxytriptamine (5-HT) or serotonin, norepinephrine (NE) and glutamate alter during ischemia and contribute to the pathophysiology of cerebral ischemia. The overall effect of serotonin in cerebral ischemia is still unclear but there are evidences that enhancement of serotonin activity in the hippocampus exerts protection against neuronal damage after ischemia. Besides, several studies showed that selective serotonin reuptake inhibitors (SSRIs), serotonin/norepinephrine reuptake inhibitors (SNRIs) and serotonin agonists reduced cerebral infarct size and improved functional recovery after stroke. There are different mechanisms that may explain the neuroprotective effect of SSRIs such as fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram and escitalopram in cerebral ischemia. They exert antioxidant, antiapoptotic and anti-inflammatory activities which are responsible for their effectiveness in stroke. In this review, we will discuss in detail the role of serotonin in ischemia and the proposed mechanisms of the neuroprotective role of SSRIs in stroke.

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Atomoxetine, a selective norepinephrine reuptake inhibitor, improves short‐term histological outcomes after hypoxic‐ischemic brain injury in the neonatal male rat

Cited by 8 publications

References 75 publications

Switching of the Microglial Activation Phenotype Is a Possible Treatment for Depression Disorder

Switching of the Microglial Activation Phenotype Is a Possible Treatment for Depression Disorder

α-Synuclein and Noradrenergic Modulation of Immune Cells in Parkinson’s Disease Pathogenesis

Therapeutic potential of serotonin in ischemic stroke

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