Plasticity following neonatal visual cortex damage in cats

Abstract

We have used the cat visual system as a model system to investigate how remaining areas of the brain are able to take over functions that are lost following brain damage and why neonates show better behavioral recovery than adults. Anatomical studies with both anterograde and retrograde tracing methods reveal an increased projection from retina through thalamus to the posteromedial lateral suprasylvian (PMLS) extrastriate visual area of cortex in the damaged hemisphere of cats with a neonatal visual cortex (areas 17, 18, and 19; VC) lesion. No such enhanced projection is seen after an adult lesion. In addition, single-cell neurophysiological studies indicate that physiological compensation is present in PMLS cortex after a neonatal VC lesion but not after an adult lesion. The physiological compensation replaces (or maintains) properties that are characteristic of PMLS neurons; there is little or no improvement to replace the superior spatial properties of striate cortex (or areas 18 or 19) neurons that were lost. Immunohistochemical studies of the possible roles of neuronal growth factors in the compensation indicate that low- and high-affinity receptors are present that would allow several neurotrophins to influence the normal retina throughout life. Furthermore, these receptors are upregulated transneuronally following neonatal VC damage and thus could play a role in lesion-induced changes in the retina and its central projections. Ongoing studies are continuing to examine the presence of neurotrophins and their receptors in the retina and brain during normal development and after VC damage. In addition, studies of the effects of administering neuronal growth factors are underway to determine whether compensation for VC damage can be improved in neonates or even be produced in adults.Key words: visual cortex, neural plasticity, brain damage, neurotrophic substances, neonatal lesion.