Jingi Yang - PhD Candidate, Neuroscience Graduate Program
The magnocellular and parvocellular pathways are the major parallel information processing streams of the early visual system. Signals relayed by these pathways from the retina to the dorsal lateral geniculate nucleus (dLGN), and then to primary visual cortex (V1) are critical for visual image processing and representation. When any of these pathways are disrupted, loss of vision occurs. The structure and function of each pathway have been well characterized. However, little is known about neurophysiological changes in these pathways following injury, such as in V1 stroke or retinal disease.
Previous work in non-human primate models of glaucoma suggests that there is a greater loss of cytochrome oxidase reactivity in parvocellular compared to magnocellular layers of the dLGN (Crawford et al., 2001, Sasaoka et al., 2008), suggesting stream-specific effects of retinal ganglion cell (RGC) degeneration. Furthermore, previous work in non-human primate models of V1 damage suggests relative preservation of visually responsive magnocellular neurons in the dLGN after long-term V1 damage (Yu et al., 2018), and visual training-induced recovery in occipital cortical stroke patients is more effective with motion stimuli, i.e., stimuli that activate the magnocellular stream. My thesis aimed to understand whether functional plasticity in the early visual pathways following cortical or retinal damage is stream-specific.
We hypothesized that both RGC loss and V1 lesions caused by stroke could differentially affect the magnocellular or parvocellular pathways. In the first study of an animal (ferret) model of RGC loss, I examined the impact of the retinal excitotoxic lesions on the physiological response properties of dLGN neurons. Although the majority of contralesional transient and sustained dLGN neurons lost tuning to contrast, sustained neurons had longer response latencies, greater variability in their responses to visual stimuli, and greater changes in their tuning preferences compared to transient neurons. In the second study of visual training-induced recovery in human stroke patients, I showed that adaptive training with static, drifting, or flickering Gabor patches of progressively lower contrasts improved contrast sensitivity for both orientation and motion discrimination in cortically-blind (vision loss due to V1 stroke) participants; however, normal contrast sensitivity was not recovered in any participant. In summary, this work suggests that: (1) More RGCs in the X (parvocellular-like) stream than those in the Y (magnocellular-like) stream degenerate following kainic acid injections into the eye, (2) sustained (parvocellular-like) neurons in the ferret dLGN appear to be less functionally resistant to degeneration 7 days following retinal lesions compared to transient (magnocellular-like) dLGN neurons, (3) lesion to V1 induces a rapid and severe impairment of contrast sensitivity for orientation and motion direction discrimination in the affected hemifield, (4) adaptive training with stimuli containing higher temporal frequencies, optimal for magnocellular pathway, is not more effective than static stimuli. Together, these findings suggest that post-injury functional plasticity in the early visual pathways depends not only on the parallel streams but also on the location of the injury and the type of the injury.
Jul 03, 2024 @ 1:00 p.m.
Medical Center | K-207 (2-6408)
Host: Advisors: Farran Briggs, PhD & Krystel Huxlin, PhD