Preprint Review Version 1 This version not peer reviewed

Complementariness and Functional Parcellation of Neurotrophin Actions on the Oculomotor System

Version 1 : Received: 6 October 2016 / Approved: 7 October 2016 / Online: 7 October 2016 (09:51:38 CEST)

A peer-reviewed article of this Preprint also exists.

Benítez-Temiño, B.; Davis-López de Carrizosa, M.A.; Morcuende, S.; Matarredona, E.R.; de la Cruz, R.R.; Pastor, A.M. Functional Diversity of Neurotrophin Actions on the Oculomotor System. Int. J. Mol. Sci. 2016, 17, 2016. Benítez-Temiño, B.; Davis-López de Carrizosa, M.A.; Morcuende, S.; Matarredona, E.R.; de la Cruz, R.R.; Pastor, A.M. Functional Diversity of Neurotrophin Actions on the Oculomotor System. Int. J. Mol. Sci. 2016, 17, 2016.

Journal reference: Int. J. Mol. Sci. 2016, 17, 2016
DOI: 10.3390/ijms17122016

Abstract

Neurotrophins play a principal role in neuronal survival and differentiation during development, but also in the maintenance of appropriate adult neuronal circuits and phenotypes. In the oculomotor system, we have demonstrated that neurotrophins are key regulators of developing and adult neuronal properties, but with peculiarities depending on each neurotrophin. For instance, the administration of NGF, BDNF or NT-3 protects neonatal extraocular motoneurons from cell death after axotomy, but only NGF and BDNF prevent the downregulation in ChAT. In the adult, in vivo recordings of axotomized extraocular motoneurons have demonstrated that the delivery of NGF, BDNF or NT-3 recovers different components of the firing discharge activity of these cells, with some particularities in the case of NGF. All neurotrophins have also synaptotrophic activity, although to different degrees. Accordingly, neurotrophins can restore the axotomy-induced alterations acting selectively on different properties of the motoneuron. In this review we summarize these evidences and discuss them in the context of other motor systems.

Subject Areas

Trophic factors; nervous system; development; plasticity; axotomy

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