Experimental neurology
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Experimental neurology · Dec 2004
The effect of brain-derived neurotrophic factor on sensory and autonomic function after lingual nerve repair.
Brain-derived neurotrophic factor (BDNF) is important in the response to peripheral nerve injury and may enhance regeneration. We have assessed its role in the functional recovery of sensory afferents and autonomic efferents after repair of the chorda tympani and lingual nerves in the cat. Six months after entubulation repair, with or without the incorporation of BDNF at the repair site, the recovery of secretomotor and vasomotor efferents was determined by recording salivary flow from the submandibular gland and temperature changes on the tongue surface, each evoked by stimulation of the repaired nerve. ⋯ The conduction velocity of afferents in the lingual nerve was also lower, but the mechanoreceptive field size was higher. Thus, despite its known trophic role in the gustatory system, BDNF had not enhanced recovery of these or other fibre populations. We conclude that the application of BDNF to a site of lingual nerve repair has a negative effect on the long-term outcome.
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Experimental neurology · Dec 2004
Comparative StudyModification of the brain-derived neurotrophic factor gene: a portal to transform mesenchymal stem cells into advantageous engineering cells for neuroregeneration and neuroprotection.
Multipotential mesenchymal stem cells (MSCs) are ideal seed cells for recruiting the loss of neural cells due to their strong proliferative capacity, easy acquisition, and considerable tolerance of genetic modifications. After transduction of brain-derived neurotrophic factor (BDNF) gene via recombinant retroviral vectors into the human MSCs, nearly 100% of cells expressed BDNF (which were therefore transformed into BNDF-MSCs) as detected by immunocytochemistry, and the quantity of BDNF in the culture medium was increased by approximately 20,000-fold. In spite of the genomic integration of an exogenous gene, BDNF-MSCs did not present any structural aberration in the chromosomes. ⋯ Compared with the MSCs induced by both RA and BDNF, BDNF-MSCs survived in significantly greater number in the induction medium, and also more cells were induced into neuron-like cells (NeuN, P < 0.01) and oligodendrocyte-like cells (O4, P < 0.05). We suppose that, once engrafted into human central nervous system, the BDNF-MSCs would not only recruit the neuronal losses, but also provide, by way of paracrine, large quantities of BDNF that effectively perform the functions of neuroprotection and neuroregeneration, promoting the activation of endogenous neural stem/progenitor cells and their chemotactic migration. On the other hand, the BDNF-MSCs that can survive in the host environment and differentiate subsequently into functional mature cells may also serve as specifically targeting vectors for ex vivo gene therapy.
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Experimental neurology · Dec 2004
Unilateral ischemic sensorimotor cortical damage in female rats: forelimb behavioral effects and dendritic structural plasticity in the contralateral homotopic cortex.
Previous studies in male rats with unilateral sensorimotor cortical (SMC) damage have demonstrated dendritic structural plasticity in the contralateral homotopic cortex and an enhancement of skilled reaching performance in the forelimb ipsilateral to the lesion compared to sham-operated rats. The purpose of this study was to determine if these findings could be replicated in an ischemic lesion model in female rats. Female rats were given sham operations or unilateral ischemic (endothelin-1 induced) damage in the forelimb representation area of the SMC opposite their preferred forelimb. ⋯ Additionally, there were major laminar-dependent increases in the surface density of MAP2 IR dendrites in the cortex opposite lesions and trained limbs. These findings in female rats are consistent with the dendritic and behavioral changes previously found in male rats. They extend these previous findings by indicating that lesion size is an important variable in the enhancement of reaching performance.