Atomoxetine Protects Against NMDA Receptor-mediated Hippocampal Neuronal Death Following Transient Global Cerebral Ischemia

Abstract

These results show that pretreatment with ATX protected against ischemic neuronal via inhibition of ischemia-induced excitotoxicity at early time following transient global cerebral ischemia.

Improved HCN channels in pyramidal neurons and their new expression levels in pericytes and astrocytes in the gerbil hippocampal CA1 subfield following transient ischemia

“…Numerous factors participate in the process of the tgCI-induced DND. For example, glutamate-mediated excitotoxicity, oxidative stress and neuroinflammatory process including activation of glial cells are involved in DND (2-6).…”

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

“…Atomoxetine administration has been demonstrated to rapidly and persistently increase the extracellular NE concentration in the rat brain (Swanson et al, 2006). Although the beneficial effects of atomoxetine were reported in animal models of traumatic brain injury and cerebral ischemia (Reid and Hamm, 2008; Park et al, 2015, 2017), the therapeutic effect of the enhancement of NE using atomoxetine against HI insult in the developing brain is unknown. In the present study, we demonstrated that atomoxetine enhanced neuronal survival against HI insult in the P7 rat brain, which was similar to that of the late preterm human infant (Vannucci et al, 1999; Vannucci and Hurn, 2009; Tucker et al, 2009).…”

“…Atomoxetine has been used clinically for the treatment of attention‐deficit hyperactivity disorder (ADHD) in children and adolescents (Garnock‐Jones and Keating, 2009). In addition, atomoxetine also exhibits neuroprotective effects in experimental animal models of traumatic injury and cerebral ischemia (Reid and Hamm, 2008; Park et al, 2015, 2017). In contrast, the potential benefits of atomoxetine for the treatment of hypoxic‐ischemic insult, especially in the developing brain, have been much less investigated.…”

Pre-treated Populus tomentiglandulosa extract inhibits neuronal loss and alleviates gliosis in the gerbil hippocampal CA1 area induced by transient global cerebral ischemia

“…However, therapeutic effects of PTE against tGCI has not yet been investigated. Therefore, in the present study, we examined neuroprotective effects of PTE in the gerbil hippocampal CA1 subjected to 5 minutes of tGCI and found that many of pyramidal neurons survived in the ischemic CA1 of gerbils pre-treated with 200 mg/kg PTE when we examined the CA1 pyramidal cells using CV staining and NeuN immunohistochemistry, which are universally used staining techniques for examining neuronal death in the brain [ 1 19 ]. This finding is the first in proving neuroprotective effects of the P. tomentiglandulosa against tGCI.…”

“…Transient global cerebral ischemia (tGCI), which is caused by lack of blood supply to the brain, results in irreversible neuronal death in venerable regions of the brain, such as the hippocampus and cerebral cortex [ 1 2 ]. The hippocampus is extremely sensitive to cerebral ischemic injury [ 3 ].…”