http://nnr.sagepub.com/content/early/2015/04/04/1545968315572389.abstract?
- William Almaguer-Melian, PhD1
- Daymara Mercerón-Martínez, MSc2
- Nancy Pavón-Fuentes, PhD1
- Esteban Alberti-Amador, PhD1
- Rilda Leon-Martinez1
- Nuris Ledón, PhD3
- Susana Delgado Ocaña4
- Jorge A. Bergado Rosado, PhD1
- 1Centro Internacional de Restauración Neurológica, La Habana, Cuba
- 2Centro de Neurociencias de Cuba, La Habana, Cuba
- 3Centro de Inmunología Molecular, La Habana, Cuba
- 4Universidad de La Habana, La Habana, Cuba
- Jorge A. Bergado Rosado, Centro Internacional de Restauración Neurológica, Ave 25, No. 15805, Playa 11300, La Habana, Cuba. Email: bergado@neuro.ciren.cu
Abstract
Background. Erythropoietin (EPO) upregulates the mitogen activated protein kinase (MAPK) cascade, a central signaling pathway in cellular
plastic mechanisms, and is critical for normal brain development. Objective.
We hypothesized that EPO could modulate the plasticity mechanisms
supporting spatial memory recovery in fimbria-fornix–transected
animals. Methods. Fimbria-fornix was transected in 3 groups of rats. Seven days later, EPO was injected daily for 4 consecutive days within
10 minutes after training on a water maze task. Results.
Our results show that EPO injections 10 minutes after training produced
a substantial spatial memory recovery in fimbria-fornix–lesioned
animals. In contrast, an EPO injection shortly
after fimbria-fornix lesion surgery does not promote spatial-memory
recovery.
Neither does daily EPO injection 5 hours after the
water maze performance. EPO, on the other hand, induced the expression
of plasticity-related genes like arc and bdnf, but this effect was independent of training or lesion. Conclusions.
This finding supports our working hypothesis that EPO can modulate
transient neuroplastic mechanisms triggered by training
in lesioned animals. Consequently, we propose that
EPO administration can be a useful trophic factor to promote neural
restoration
when given in combination with training.
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