Fluoxetine attenuates kainic acid-induced neuronal cell death in the mouse hippocampus

Jin, Young–Joo; Lim, Choon Woo; Kim, Seung-Woo; Park, Ju‐Young; Seo, Ji-Seon; Han, Pyung Lim; Yoon, Sung Hwa; Lee, Ja-Kyeong

doi:10.1016/j.brainres.2009.04.053

Cited by 88 publications

(47 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Of interest, inhibition of VDAC or Na þ /Ca 2þ channels by fluoxetine is neuroprotective (Nahon et al, 2005;Ouardouz et al, 2005;Shimizu et al, 1999). Furthermore, fluoxetine attenuates kainate-induced neuronal cell death in the mouse hippocampus ( Jin et al, 2009). Fluoxetine activates the dopamine-and cAMP-regulated phosphoprotein of MW 32 kD (DARPP-32), and increases the phosphorylation state and efficacy of several ion channels and ionotropic receptors, such as AMPA receptors.…”

Section: Figmentioning

confidence: 99%

Fluoxetine Increases Hippocampal Neurogenesis and Induces Epigenetic Factors But Does Not Improve Functional Recovery after Traumatic Brain Injury

Wang

Neumann

Hansen

et al. 2011

Journal of Neurotrauma

View full text Add to dashboard Cite

The selective serotonin reuptake inhibitor fluoxetine induces hippocampal neurogenesis, stimulates maturation and synaptic plasticity of adult hippocampal neurons, and reduces motor/sensory and memory impairments in several CNS disorders. In the setting of traumatic brain injury (TBI), its effects on neuroplasticity and function have yet to be thoroughly investigated. Here we examined the efficacy of fluoxetine after a moderate to severe TBI, produced by a controlled cortical impact. Three days after TBI or sham surgery, mice were treated with fluoxetine (10 mg/kg/d) or vehicle for 4 weeks. To evaluate the effects of fluoxetine on neuroplasticity, hippocampal neurogenesis and epigenetic modification were studied. Stereologic analysis of the dentate gyrus revealed a significant increase in doublecortin-positive cells in brain-injured animals treated with fluoxetine relative to controls, a finding consistent with enhanced hippocampal neurogenesis. Epigenetic modifications, including an increase in histone 3 acetylation and induction of methyl-CpG-binding protein, a transcription factor involved in DNA methylation, were likewise seen by immunohistochemistry and quantitative Western immunoblots, respectively, in brain-injured animals treated with fluoxetine. To determine if fluoxetine improves neurological outcomes after TBI, gait function and spatial learning and memory were assessed by the CatWalkassisted gait test and Barnes maze test, respectively. No differences in these parameters were seen between fluoxetine-and vehicle-treated animals. Thus while fluoxetine enhanced neuroplasticity in the hippocampus after TBI, its chronic administration did not restore locomotor function or ameliorate memory deficits.

show abstract

Section: Figmentioning

confidence: 99%

Fluoxetine Increases Hippocampal Neurogenesis and Induces Epigenetic Factors But Does Not Improve Functional Recovery after Traumatic Brain Injury

Wang

Neumann

Hansen

et al. 2011

Journal of Neurotrauma

View full text Add to dashboard Cite

show abstract

“…It appears that khellin extracts have some antimicrobial activity; this might be attributable to both the khellin and visnagin constituents, which both seem to have antifungal, antibacterial, and antiviral activity [25]. In addition, several reports have demonstrated that drugs or compounds having an anti-inflammatory effect can show a neuroprotective effect [4,26,27]. Thus, we examined the effect of visnagin on proinflammatory mediators expression induced by KA.…”

Section: Discussionmentioning

confidence: 99%

“…glutamate), which are massively released as a consequence of energy depletion and which result in excitotoxic neuron death [2,3]. Recent studies have demonstrated that the KA-induced neuronal death is associated with the activation of microglia and astrocytes in the hippocampus, and that these processes are induced by enhanced reactive oxygen species (ROS) production and cytokine expressions [4,5]. The microglia also can be detected using the complement receptor type 3 (OX-42) IR.…”

Section: Introductionmentioning

confidence: 99%

“…In addition, recent studies have demonstrated that inflammatory and apoptotic processes contribute to the later stages of the damage induced by various brain injuries, and that these detrimentally affect neurologic outcome [5,8]. Among them, it has been reported well that pro-inflammatory mediators such as IL-1β, TNF-α, IL-6, and COX-2 can lead to deteriorative effect in the brain, and KA can trigger an aberrant inflammatory cytokine response by microglial cells and accelerated disease progression [4].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neuroprotective Effect of Visnagin on Kainic Acid-induced Neuronal Cell Death in the Mice Hippocampus

Kwon

Lee

Park

et al. 2010

Korean J Physiol Pharmacol

View full text Add to dashboard Cite

Visnagin (4-methoxy-7-methyl-5H-furo[3,2-g][1]-benzopyran-5-one), which is an active principle extracted from the fruits of Ammi visnaga, has been used as a treatment for low blood-pressure and blocked blood vessel contraction by inhibition of calcium influx into blood cells. However, the neuroprotective effect of visnagin was not clearly known until now. Thus, we investigated whether visnagin has a neuroprotective effect against kainic acid (KA)-induced neuronal cell death. In the cresyl violet staining, pre-treatment or post-treatment visnagin (100 mg/kg, p.o. or i.p.) showed a neuroprotective effect on KA (0.1 μg) toxicity. KA-induced gliosis and proinflammatory marker (IL-1β, TNF-α, IL-6, and COX-2) inductions were also suppressed by visnagin administration. These results suggest that visnagin has a neuroprotective effect in terms of suppressing KA-induced pathogenesis in the brain, and that these neuroprotective effects are associated with its anti-inflammatory effects.

show abstract

“…Fluoxetine may affect articular inflammation via inhibition of production of NO and PGE2 [9] and it inhibits NO production in LPS-induced microglia BV2 cells [19,20]. Fluoxetine attenuates COX-2 induction to suppress kainic acid-induced gliosis and inflammation in the mouse hippocampus [21] and to be against colon cancer development in epithelial and stromal areas in rats [22]. Immunomodulatory effect of fluoxetine on human T lymphocyte function is related to inhibition of COX-2 induction [23].…”

Section: Discussionmentioning

confidence: 99%

Glycogen synthase kinase-3β regulates anti-inflammatory property of fluoxetine

Ting

et al. 2012

International Immunopharmacology

View full text Add to dashboard Cite

Fluoxetine attenuates kainic acid-induced neuronal cell death in the mouse hippocampus

Cited by 88 publications

References 31 publications

Fluoxetine Increases Hippocampal Neurogenesis and Induces Epigenetic Factors But Does Not Improve Functional Recovery after Traumatic Brain Injury

Fluoxetine Increases Hippocampal Neurogenesis and Induces Epigenetic Factors But Does Not Improve Functional Recovery after Traumatic Brain Injury

Neuroprotective Effect of Visnagin on Kainic Acid-induced Neuronal Cell Death in the Mice Hippocampus

Glycogen synthase kinase-3β regulates anti-inflammatory property of fluoxetine

Contact Info

Product

Resources

About