Prof Manuel Vidal-Sanz, MD, PhD, FARVO, trained as an MD (University of Valladolid, 1979) and obtained a first PhD degree from the Complutense University of Madrid, 1984. He then became a Medical Research Council of Canada Postdoctoral Fellow under the supervision of Albert J Aguayo, at McGill University (1984-1991) (Montreal, Canada) where he obtained a PhD in Neuroscience in 1990. In 1991 he was appointed Research staff member at the Cajal Institute (Madrid, Spain), in 1992 he started the Laboratory of Experimental Ophthalmology at the Faculty of Medicine (Murcia University, Murcia, Spain) and became full professor (July 1996) to teach neurophysiology of the visual system.

Dr Vidal-Sanz has made contributions to the field of vision research. His main research interests are neurodegeneration, neuroprotection and repair of the adult mammalian visual system. In the late 80’s, his work provided seminal contributions to the field, demonstrating for the first time the capacity of adult mammalian central nervous system neurons to regenerate their axons, re-innervate their target and establish new synaptic connections that would persist for long periods of time and would relay visual information onto other retinorecipient nuclei. This was published in a series of papers in collaboration with the group of Albert J. Aguayo at McGill University (Keirstead et al., 1989; Vidal-Sanz et al., 1987, 1991, 1993) and was further extended later in Spain (Whiteley et al., 1998; Avilés-Trigueros et al., 2000; Vidal-Sanz et al., 2002).

Manuel Vidal-Sanz also developed a special interest in the problem injury-induced cell death and its prevention, and his contributions have also been seminal with the first observation of the capacity to prevent injury induced retinal ganglion cell (RGC) death, something we know now as Neuroprotection. For this purpose his Laboratory has studied retinal degeneration and characterized several models of injury-induced neuronal death in the adult rodent retina. A first model was axotomy-induced retinal ganglion cell (RGC) loss either by a complete optic nerve division or a complete optic nerve crush at different distances from the cell somata, as well as its functional implications in the adult rodent retina. The effects of transient ischemia of the retina induced by increased intraocular pressure (Sellés et al., 1996) or by selective ligature of the ophthalmic vessels (Lafuente et al., 2002) on the survival and function of the RGC population as well as on its main retinorecipient target region were also characterized in detail in several publications.

These previous studies served as basis to investigate the effects of several molecules to prevent or slow down the process of injury-induced retinal ganglion cell death. This was investigated initially for the axotomy-induced RGC death paradigm, and later the neuroprotective effects of several molecules against the effects of transient ischemia-induced RGC loss, including several alpha-2 receptor agonists, were also studied in detail.

The effects of injury induced by chronic elevation of the intraocular pressure has been studied (Vidal-Sanz et al., 2012, 2015) in adult albino rats (Salinas-Navarro et al., 2010) and mice (Salinas-Navarro et al., 2009; Cuenca et al., 2010; Nguyen et al., 2011). The effects of this type of injury on the contralateral, unaffected eye were also reported for the first time (Ramírez et al., 2010; Gallego et al., 2012; de Hoz et al., 2013; Rojas et al., 2014).

More recently the population of intrinsically photosensitive RGCs in adult rats and mice were characterized using modern neuroanatomical tools and their response to a number of retinal injuries were studied in detail (Vidal-Sanz et al., 2015, 2017).

In parallel Prof. Manuel Vidal-Sanz’s laboratory has contributed by developing a number of techniques that have allowed detailed quantitative anatomical and topological studies, including: i) a method to produce complete optic nerve transection and grafting a segment of peripheral nerve as a bridge between the retina and its main retinorecipient target regions in the brain of the adult rat (Vidal-Sanz et al., 1993, 2002); ii) a method to label retrogradely the entire RGC population with fluorescent and persistent tracers (Vidal-Sanz et al., 1988; Peinado-Ramón et al., 1996; Sellés et al., 1996; Vidal-Sanz et al., 2000); iii) the identification of Brn3a as a molecular marker that permits identification of na?ve and injured retinal ganglion cells in adult rats (Nadal-Nicolás et al., 2009, 2012, 2014) and mice (Galindo-Romero et al., 2011); iv) a method to induce transient ischemia by increased intraocular pressure (Sellés-Navarro et al., 1996) or by selective ligature of the ophthalmic vessels (Lafuente et al., 2002); v) the use of orthograde tracers to quantify the retinotectal innervation of the adult rat in control and injured visual systems (Avilés-Trigueros et al., 2003; Mayor-Torroglosa et al., 2005; Vidal-Sanz et al., 2007); vi) a method to count automatically the entire population of neurons in in the ganglion cell layer and to represent topologically their distribution, including RGCs, displaced amacrine cells and intrinsic photosensitive RGCs in adult rats (Salinas-Navarro et al., 2009a; Galindo-Romero et al., 2013; Nadal-Nicolás et al., 2009, 2012, 2014, 2015) and mice (Salinas-Navarro et al., 2009b; Sánchez-Migallón et al., 2016), or the population of cones in adult rats (Ortín-Martínez et al., 2010; 2014b; 2015) and mice (Ortín-Martínez et al., 2014a).

Dr Vidal-Sanz has been continuously funded by Spanish, European, and International granting agencies since 1991. At the national level, Dr Vidal-Sanz served four years (2006-2010) in the Spanish National Board for evaluation of the scientific activity, and in the Valencian Community, the Bask Community and the Castilla y León Community boards for evaluation of the academic activity. Manuel Vidal-Sanz acts as a regular reviewer and serves in the editorial board of several peer reviewed journals.

Manuel has been an active member of ISER for many years and has attended most of the ISER meetings for the last twelve years. Prof. Vidal-Sanz serves on grant review panels for Spanish and International Granting agencies. Prof. Vidal-Sanz has served as Treasurer and member of the Council of the Spanish Society for Neuroscience and in 1997 was a Visiting Professor at the Department of Developmental Neuroscience of Uppsala University (Sweden). His contributions to education and research are underscored by his appointment as Head of the Department of Ophthalmology of Murcia University (May 1997-April 2006) and later as Vice-Chancellor of Health Sciences and Institutional Relations of Murcia University (May 2006-May 2014). As Vice-Chancellor he fostered the construction of a new Health Sciences Campus and the organization of a Regional Biomedical Research Institute.

Prof. Vidal-Sanz has published a total of 125 articles in peer reviewed journals. His work has been cited over 6,330 times and has an h-index of 46 and a Fh parameter of 1,19 [Searched: WEB of Science; ALL DATA BASES; Author=(Vidal-Sanz M* OR VIDAL$SANZ M) Refined by: [excluding] Document Types=(ABSTRACT)].

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Terms of Appointment: August 2020 - July 2022;  August 2022 - July 2024