Experimental neurology
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Experimental neurology · Feb 2000
Growth factors in combination, but not individually, rescue rd mouse photoreceptors in organ culture.
The rd mouse retina is an animal model for human retinal dystrophy in which the rod photoreceptors undergo apoptosis during the first 4 weeks in vivo or in organ culture. We have examined the effect of different families of trophic factors on the survival of rd mouse photoreceptors in organ culture. Retinas were harvested from rd mice at postnatal day 2 and grown in organ culture for 27 days in vitro (DIV) in DMEM with 10% fetal calf serum. ⋯ A significant increase in photoreceptor survival was seen with forskolin added to CNTF, but not to BDNF, FGF2, or GDNF. These results demonstrate that trophic factors promote photoreceptor survival through a synergistic interaction. Increased understanding of receptor interactions and signaling pathways may lead to a potential therapeutic role for combinatorial trophic factors in treatment of photoreceptor dystrophies.
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Experimental neurology · Feb 2000
Nerve guides seeded with autologous schwann cells improve nerve regeneration.
This study evaluates the ability of Schwann cells (SCs) transplanted into a nerve guide to improve regeneration and reinnervation after sciatic nerve resection and repair, leaving a 6-mm gap, in the mouse. SCs were isolated from predegenerated adult sciatic nerves and expanded in culture using a chemically defined medium. Syngeneic, isogeneic, and autologous SCs were suspended in Matrigel and seeded in resorbable, permeable poly(l-lactide-co-epsilon-caprolactone) guides at 150,000 cells/tube. ⋯ Syngeneic SCs did not improve regeneration with respect to acellular guides. Prelabeled transplanted SCs were found to survive into the guide 1-3 months after implantation, to a larger number when they were autologous than syngeneic. Cellular prostheses composed of a resorbable guide seeded with autologous SCs appear as an alternative for repairing long gaps in injured nerves, approaching the success of autografts.
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Experimental neurology · Feb 2000
Continuous infusion of cyclosporin A postinjury significantly ameliorates cortical damage following traumatic brain injury.
Traumatic brain injury (TBI) results in the rapid necrosis of cortical tissue at the site of injury. In the ensuing hours and days, secondary injury exacerbates the original damage resulting in significant neurological dysfunction. Recent reports from our lab demonstrate that a bolus injection of the immunosuppressant cyclosporin A (CsA) is neuroprotective following TBI. ⋯ All animals receiving CsA demonstrated a significant reduction in lesion volume, with the highest dose offering the most neuroprotection (74% reduction in lesion volume). These results extend our previous findings and demonstrate that chronic infusion of CsA is neuroprotective following TBI. These findings also suggest that the mechanisms responsible for tissue necrosis following TBI are amenable to manipulation.