LGN activity patterns during ocular dominance plasticity in vivo

Abstract

Perturbations of sensory experience in young animals are known to cause lasting changes in adult brain function. For example, monocular visual deprivation by lid closure (MC) leads to a loss of cortical responsiveness of the deprived eye and a concomitant visual impairment. This ocular dominance (OD) plasticity is a well-studied model of experience-dependent cortical plasticity. While much is known about the anatomical, physiological and biochemical changes that occur in primary visual cortex following OD plasticity, the input patterns that lead to these changes have not been characterized. Visual input travels from the retina through the dorsal lateral geniculate nucleus (dLGN) of the thalamus and then into visual cortex. Several models of the thalamic activity patterns which drive OD plasticity have been proposed, but the assumptions about the pattern and amount of input activity from thalamus to cortex during deprivation have not been experimentally validated. Therefore, we performed extracellular recordings from the dLGN of animals during periods of visual manipulation. Contrary to previous hypotheses, the present findings demonstrate that MC does not alter the overall firing rate of neural activity in the dLGN. Instead, MC alters the pattern of neural spike trains such that there is a decrease in simultaneous firing of neighboring neurons. Moreover, the elimination of visual input from the retina, a form of deprivation which does not lead to deprived-eye depression, leads to a dramatic increase in thalamic bursting. Additionally, there are subtle qualitative differences between dLGN activity in juveniles and adults during MC, and this may contribute to differences in OD plasticity with age.