The ability of neurons to undergo experience-dependent changes in form and function early in an organism's development is an area of intense research. The seminal studies of Hubel and Wiesel established the feline (Wiesel & Hubel, 1963) and later the macaque visual systems (Hubel et al., 1977) as premier animal models for investigating experienced-based neuroplasticity in developing animals. They demonstrated that the effects of visual deprivation on ocular dominance (a hallmark property of neurons in the early visual system) depend not only on the duration of deprivation, but also on the timing. Deprivation early in an animal's postnatal development can induce long-lasting changes in ocular dominance, resulting in commensurate visual deficits, while similar deprivation in older animals produces little change These and other lines of investigation support the notion that while younger animals have an intrinsic capability for experience-dependent developmental neuroplasticity, this capability is greatly diminished or absent in adults. In subsequent years, however, a multitude of studies have demonstrated adult mammals can in fact display experience-dependent structural and functional changes following visual deprivation (Darian-Smith & Gilbert, 1995; Yamahachi et al., 2009) and, in some cases, subcortical changes as well (Moore et al., 2011). At present, the extent, speed, magnitude and other properties of adult neuroplasticity remain imperfectly understood. Understanding the nature of adult neuroplasticity is extremely important for the acute and long-term treatment of adults suffering from brain damage, such as due to traumatic brain injury or prolonged ischaemia resulting from stroke. While feline and non-human primates remain the dominant models for investigations of adult visual system structure and function, other animals such as mice and ferrets possess attributes that make them advantageous for studying developmental and adult neuroplasticity. For instance, as opposed to cats and primates, ferrets are born relatively immature, making them an attractive model for investigating developmental neuroplasticity (Chapman & Stryker, 1993). Over the past decade, the murine model of vision has become increasingly prominent, in part due to practical reasons such as expense and availability. More important, however, is the abundance of molecular tools permitting advanced visualization and targeted manipulation of the developing and adult mouse nervous system (Luo et al., 2008; Huberman & Niell, 2011). For many lines of inquiry, these advantages outweigh the disadvantages of studying vision in mice, chief of which is perhaps their extremely poor spatial vision (Prusky & Douglas, 2004). Moreover, the murine model does not yet benefit from the vast experimental literature amassed for the feline and primate models in the wake of Hubel and Wiesel's pioneering studies. In order for the mouse to become a dominant animal model of vision, many classic experiments will need to be repeated, with similarities and differences noted for future investigations. Along these lines, a recent study by Smolders et al. (2016) investigates how adult mouse visual cortex and superior colliculus respond to permanent laser-induced retinal lesions. They estimated spatiotemporal changes in lesion projection zones by calculating optical density values of zif268, a transcription factor associated with ongoing neural activity. They demonstrate that monocular retinal lesions result in topographic decreases in zif268 expression patterns in contralateral primary visual (V1) and extrastriate cortical areas. Within 3 weeks post-lesion, cortical zif268 expression returned to normal, with areas along the border of the lesion projection zone recovering sooner. Interestingly, higher visual areas demonstrated faster recovery of normal zif268 expression. This might be expected given that neurons further along in the cortical processing hierarchy typically have larger receptive fields and thus integrate visual information originating from larger swaths of retina. Notably, retinal lesions resulted in an apparently permanent lesion projection zone in the superior colliculus, a subcortical zone that receives direct retinal input. The investigation by Smolders et al. (2016) draws heavily on methods applied in other species to investigate adult neuroplasticity (Arckens et al., 2000; Hu et al., 2009), and more work is needed to delineate the ‘functional’ reorganization associated with focal visual deprivation in the mouse. An examination of visual responses and receptive field properties in the lesion projection zones would be especially insightful. Because Smolders et al. (2016) examines neuroplasticity only with regard to zif268 expression, and report results similar to those found in other and arguably more suitable animal models for investigating neuroplasticity, it may be tempting to disregard the study's potential impact. Yet the importance of Smolders et al. (2016) lies ultimately in its animal model; there is little doubt that the mouse is slowly joining the ranks of cat and non-human primate in becoming a premier animal model of vision. This ascendancy is critical for the exploration of novel treatments for adult brain damage.
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Nov 3, 2021
K Tang-Wright + 9
Open Access
