Neuroprotection and reduced gliosis by atomoxetine pretreatment in a gerbil model of transient cerebral ischemia

Abstract Atomoxetine (ATX) is a non-stimulant selective norepinephrine reuptake inhibitor that is widely used for the treatment of attention-deficit/hyperactivity disorder (ADHD). In this study, we firstly examined neuroprotective effects of pre- or post-treatment with 15 and 30 mg/kg ATX against is...

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Published in:Journal of the neurological sciences 2015-12, Vol.359 (1), p.373-380
Main Authors: Park, Joon Ha, Shin, Bich Na, Chen, Bai Hui, Kim, In Hye, Ahn, Ji Hyeon, Cho, Jeong-Hwi, Tae, Hyun-Jin, Lee, Jae-Chul, Lee, Choong-Hyun, Kim, Young-Myeong, Lee, Yun Lyul, Kim, Sung Koo, Won, Moo-Ho
Format: Article
Language:English
Subjects:
Analysis of Variance
Animals
Atomoxetine
Atomoxetine Hydrochloride - therapeutic use
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Administration Schedule
Fluoresceins - metabolism
Gerbillinae
Glial activation
Glial Fibrillary Acidic Protein - metabolism
Gliosis - etiology
Gliosis - prevention & control
Hippocampus
Ischemic Attack, Transient - complications
Male
Microfilament Proteins - metabolism
Neurology
Neuroprotection
Neuroprotective Agents - therapeutic use
Phosphopyruvate Hydratase - metabolism
Selective norepinephrine reuptake inhibitor
Transient cerebral ischemia
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Summary:Abstract Atomoxetine (ATX) is a non-stimulant selective norepinephrine reuptake inhibitor that is widely used for the treatment of attention-deficit/hyperactivity disorder (ADHD). In this study, we firstly examined neuroprotective effects of pre- or post-treatment with 15 and 30 mg/kg ATX against ischemic damage in the gerbil hippocampal cornus ammonis 1 (CA1) region subjected to 5 min of transient cerebral ischemia using cresyl violet staining, neuronal nuclei immunohistochemistry and Fluoro-J B histofluorescence staining. We found that only pre-treatment with 30 mg/kg ATX protected CA1 pyramidal neurons from ischemic insult. In addition, pre-treatment with 30 mg/kg ATX, which had neuroprotective effect against ischemic damage, distinctly attenuated the activation of astrocytes and microglia in the ischemic CA1 region compared with the vehicle-treated ischemia group by glial fibrillary acidic protein (for astrocytes) and ionized calcium-binding adapter molecule 1 (for microglia) immunohistochemistry. In brief, our present results indicate that ATX has neuroprotective effect against transient cerebral ischemic insult and that the neuroprotective effect of ATX may be closely associated with attenuated glial activation.
ISSN:0022-510X
1878-5883
DOI:10.1016/j.jns.2015.11.028