This research project will describe and quantify the cellular abnormalities in the central nervous system that result from visual deprivation. The long range goal is to explain specifically which neurons are affected in visual deprivation amblyopia and the cellular nature of this deficit. The neurons of the dorsal lateral geniculate nucleus (LGNd) are positioned strategically for this type of investigation. Under conditions of monocular deprivation (MD) these cells receive input from a physiologically normal eye and send information to a highly abnormal visual cortex. LGNd cells will be studied in MD cats. The physiological properties and structure of individual geniculocortical axons will be directly related for the first time in visually deprived animals. This is being done by intracellular recording and injection of the enzyme marker substance-horseradish peroxidase (HRP) into single geniculocortical axons (from cells of both the LGNd layers innervated by the visually deprived and the non-deprived eye). The HRP fills the axon's terminal arborization in visual cortex by anterograde movement. Each axon will be evaluated for its cortical target zone, laminar distribution of the terminal boutons, cortical volume innervated and the density of innervation. These parameters will be directly related to the axon's physiological properties (including the X- vs. Y- axon classification and any abnormalities in the axon's receptive field properties). Many axon's receptive field properties will be anlalyzed for trial by trial variability of responsiveness to repeated visual stimuli. Response irregularities shown by this method would otherwise be missed with an averaging technique. These abnormalities will be related to the structural features of the individual geniculocortical axons, that have been injected with HRP.
