Brain-derived neurotrophic factor promotes survival and blocks nitric oxide synthase expression in adult rat spinal motoneurons after ventral root avulsion☆
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Artemisinin protects motoneurons against axotomy-induced apoptosis through activation of the PKA-Akt signaling pathway and promotes neural stem/progenitor cells differentiation into NeuN<sup>+</sup> neurons
2020, Pharmacological ResearchCitation Excerpt :In this study, the brachial plexus axotomy induced a significant decrease number of IB4-positive cells in DRGs, which was reversed upon artemisinin treatment denoting the impact of the treatment on the number of sensory neurons. Brachial plexus axotomy-induced deprivation of neurotrophic factors often promotes the deformation, swelling, and even apoptosis of the damaged neurons, thus affecting neuronal survival and regeneration [47–49]. As the affected axons lose their connection with the central nervous system, their survival and regeneration are dependent on the establishment of several morphological, cellular, and molecular changes [50,51].
Pathologic role of nitrergic neurotransmission in mood disorders
2019, Progress in NeurobiologyBrachial Plexus Avulsion: A Model for Axonal Regeneration Study
2015, Neural RegenerationNeuroprotective effects of mesenchymal stem cells on spinal motoneurons following ventral root axotomy: Synapse stability and axonal regeneration
2013, NeuroscienceCitation Excerpt :After axotomy at the ventral funiculus of the spinal cord, which cuts motor axons very proximally, only a few hundred microns from the cell body, about half of the population of lesioned motoneurons dies at 1–3 weeks postoperatively, differing considerably from that observed after transection of a peripheral nerve (Lindå et al., 2000). Another motoneuron proximal lesion, which has been investigated, is the VRA (Wu, 1993, 1996; Koliatsos et al., 1994; Novikov et al., 1995). Such lesions mimics brachial plexus lesions that occur in patients, mostly following high energy accidents such as motorbike crashes.
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This study was supported by the Swedish Medical Research Council (project 2886), Umeå University and Josef Anér's Foundation.