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The Role of Visual Thalamus in Residual Vision Following Loss of Retinal or Cortical Inputs

In mammals, the visual thalamus, the lateral geniculate nucleus (LGN), relays visual information from the retina to the primary visual cortex (V1) and also receives feedback from V1. Both retinal and cortical inputs are critical to processing visual information within the LGN. The role of the LGN in residual vision following loss of retinal or cortical inputs is not known. In particular, we want to explore how loss of inputs (retinal or cortical) alter the physiological responses of LGN neurons.

The first aim of this project is to expand current understanding of the impact of loss of retinal inputs on the early visual pathway by studying the visual properties of LGN neurons that are deprived of their retinal inputs. Past studies have provided evidence for reorganization of receptive fields within the LGN in the absence of retinal inputs. Beyond spatial receptive field reorganization, little is known about residual visual response properties of LGN neurons following loss of retinal inputs. We will examine LGN responses to a variety of visual stimuli and correlate visual response properties with morphological changes in the retina and LGN following death of retinal ganglion cells, the major output projection neurons of the retina. We utilize a variety of methods to quantify neurophysiological and morphological changes including multi-electrode array recordings of LGN neurons, high resolution optical coherence tomography (OCT) and fundus imaging, full-field electroretinogram (ERG) recordings, and histological tissue processing.

The second aim of this project is to study the effects of loss of cortical inputs on the neuronal responses in the LGN. Residual visual responses in the LGN following cortical occipital stroke could underlie “blindsight”, or unconscious visual capabilities. Past studies demonstrated that LGN neurons maintained receptive fields and visual responsiveness following V1 lesions. We aim to extend these studies by combining neurophysiological measurements of LGN responses with behavioral assessments of residual visual capabilities in order to directly relate residual vision to neuronal properties.

Through both aims, we can make direct comparisons of changes in LGN activity following loss of retinal or cortical inputs, which will help us further understand the role of LGN in normal vision and in blindsight. Our ultimate goal is to provide new insight into vision restoration therapies for patients who suffer from vision loss due to eye disease, like glaucoma, or visual cortical lesions following stroke.

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