Abstract:

Identifying specific RGC types may shed light on their idiosyncratic responses to neuroprotection Retinal ganglion cells (RGCs) are located in the innermost layer of the retina and are the only output retinal neurons, conveying light information to the main retinorecipient target regions of the brain responsible for the image and non-image forming visual functions. There are well over twenty RGC types, each with its own dendritic morphological and physiological characteristics, target territories and visual functions. The study of the responses of RGCs to various injury-induced or inherited retinal degenerations requires the identification of these neurons. Up to know RGCs have been identified mainly with retrograde tracers applied to their principal retinorecipient target nuclei in the brain, the superior colliculi (SCi), or to their main axonal output, the optic nerve (ON). These methods, although most efficient to label the great majority of RGCs do not allow distinction between different RGC types. Retrogradely transported tracers applied to the ON result in massive retrograde labelling of RGCs, while tracer application to the SCi labels most RGCs projecting to these nuclei as well as to neighbouring areas. Indeed, injection into the optic tract or tracer application over the SCi may result in spurious labelling of neurons in the brain located in different neighbour areas. Prof. Manuel Vidal-Sanz (Universidad de Murcia, Spain) considered that new discoveries of suitable molecular markers to identify other types of RGCs would allow deciphering and dissecting out the responses of RGCs and thus further advance our knowledge of the molecular mechanisms in each of these types that render them susceptible and/or capable of survival, amenable to rescuing intervention or axonal regeneration. Indeed, new discoveries or characterization of molecular markers for specific types of RGCs may allow further characterization of the responses of different types of RGCs to axonal injury, such as neuronal survival, axonal regeneration, synapse formation and re-establishment of function.