Neuroplasticity and behavioral effects of fluoxetine after experimental stroke
Neuroplasticity and behavioral effects of fluoxetine after experimental stroke
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实验性卒中后氟西汀的神经可塑性和行为影响
DOI:
10.3233/rnn-170725
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发表时间:
2017
影响因子:
2.8
通讯作者:
Chuansheng Zhao
中科院分区:
文献类型:
--
作者:
Yefei Sun;Xiaoyu Sun;Huiling Qu;Shanshan Zhao;Ting Xiao;Chuansheng Zhao
The brain can undergo self-repair and has the ability to compensate for functions lost after a stroke. The plasticity.of the ischemic brain is influenced by several factors including aging and pharmacotherapy. Fluoxetine is an antidepressant.which enhances serotonergic neurotransmission through selective inhibition of neuronal reuptake of serotonin. In clinical.practice, fluoxetine alleviates the symptoms of post-stroke depression (PSD), helps motor recovery in stroke patients. In animal.experiments£¬chronic administration of fluoxetine induces increased excitability of mature granule cells (GCs), enhancing.axonal and dendritic reorganization, as well as promoting neurogenesis or angiogenesis in the dentate gurus (DG), but the.effect of fluoxetine in the subventricular zone (SVZ) remains controversial. Meanwhile, chronic treatment with fluoxetine.did not reverse age-dependent suppression of proliferation cells in the DG. Interestingly, although fluoxetine has been found.to enhance neurogenesis in the DG in stroke rats, this property is not consistent with the behavioral recovery. More studies.into this issue will be required to reveal how to translate enhanced neuronal plasticity into behavioral benefits. This review.provides an update of the current knowledge about the neurogenesis and the fate of the newly generated cells after the use of.fluoxetine, as well as its ability to promote a behavioral recovery after stroke in clinical and experimental results and attempts to define the therapeutic properties of fluoxetine in regenerative neuroscience.