The Department of Ophthalmology and Visual Science
Department of Ophthalmology
The Department of Ophthalmology

Faculty Biography

 


Louvenia Carter-Dawson, Ph.D.

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Clinical and Research Interests:

  1. Primary open-angle high-tension glaucoma is one of the leading causes of blindness in the United States. In some families the disorder appears to be genetically determined. It is characterized by elevated intraocular pressure (IOP) above 21 mmHg, optic nerve head cupping, retinal ganglion cell death and elevated thresholds on visual field analysis. Since vision cannot be restored, early detection and proper treatment are essential for preservation of vision. Current treatments of lowering the intraocular pressure provide considerable benefit to prevent vision loss, but they are not always highly effective. Improved knowledge of the underlying mechanisms that contribute to the sequence of events that cause the death of ganglion cells may lead to improved treatment strategies.
  2. Our long-range objective is to understand the cascade of events that determine retinal ganglion cell injury and death in glaucoma. Current research activities in the laboratory focus on the hypothesis that glutamate is involved in the disease process particularly since vitreal glutamate was found elevated in patients with glaucoma and in animal models of the disorder (Dreyer et al., 1996; Dreyer and Lipton, 1999). High vitreal glutamate implicates changes in Müller cells since they normally remove glutamate from the extracellular space and convert it primarily to glutamine. This activity of Müller cells prevents prolonged neuronal exposure to glutamate and subsequent excitotoxic damage. Our studies investigate the functional state and activity of Müller cells in the transport and metabolism of glutamate in primates with experimental glaucoma.

Publications (selected):

  1. Ganglion cell losses underlying visual field defects from experimental glaucoma Harwerth RS, Carter-Dawson L, Shen F, Smith EL and Crawford MLJ. Invest. Ophthalmol. Vis Sci. 40: 2242, 1999. PURPOSE: To investigate the relationship between ganglion cell losses and visual field defects caused by glaucoma. METHODS: Behavioral perimetry and histology data were obtained from 10 rhesus monkeys with unilateral experimental glaucoma that was induced by argon laser treatments to their trabecular meshwork. After significant visual field defects had developed, the retinas were collected for histologic analysis. The ganglion cells were counted by light microscopy in cresyl violet-stained retina sections, and the percentage of ganglion cell loss (treated to control eye counts) was compared with the depth of visual field defect (treated to control eye thresholds) at corresponding retinal and perimetry test locations. Sensitivity losses as a function of ganglion cell losses were analyzed for Goldmann III, white and Goldmann V, and short- and long-wavelength perimetry test stimuli. RESULTS: The relationship between the proportional losses of ganglion cells and visual sensitivity, measured with either white or colored stimuli, was nonlinear. With white stimuli, the visual sensitivity losses were relatively constant (approximately 6 dB) for ganglion cell losses of less than 30% to 50%, and then with greater amounts of cell loss the visual defects were more systematically related to ganglion cell loss (approximately 0.42 dB/percent cell loss). The forms of the neural-sensitivity relationships for visual defects measured with short- or long-wavelength perimetry stimuli were similar when the visual thresholds were normalized to compensate for differences in expected normal thresholds for white and colored perimetry stimuli. CONCLUSIONS: Current perimetry regimens with either white or monochromatic stimuli do not provide a useful estimate of ganglion cell loss until a substantial proportion have died. The variance in ganglion cell loss is large for mild defects that would be diagnostic of early glaucoma and for visual field locations near the fovea where sensitivity losses occur relatively late in the disease process. The neural-sensitivity relationships were essentially identical for both white and monochromatic test stimuli, and it therefore seems unlikely that the higher sensitivity for detecting glaucoma with monochromatic stimuli is based on the size-dependent susceptibility of ganglion cells to injury from glaucoma.
  2. Glutamine immunoreactivity in Müller cells of monkey eyes with experimental glaucoma
    Carter-Dawson L, Shen F, Harwerth RS, Smith EL, Crawford MLJ and Chuang A. Exp. Eye Res. 66:537, 1998. The action of glutamate in retina is largely terminated through rapid uptake by Müller cells and subsequent conversion primarily to glutamine. Glutamine, transferred from Müller cells to neurons, serves as a precursor for the formation of glutamate in neurons completing the glutamate-glutamine cycle. In a monkey model of high-tension glaucoma, we have examined glutamine immunoreactivity in the Müller cell as well as the number of Müller cells to determine whether the activity of these cells in the glutamate-glutamine cycle is affected, particularly since high vitreal glutamate has been reported in glaucoma. Unilateral glaucoma was induced in three monkeys by argon laser application to the trabecular meshwork. LR White sections of retina from the temporal mid-periphery (about 23 degrees) and the parafovea (central 3 degrees) were immunolabeled for glutamine using immunogold and silver intensification. The percentage difference in labeling intensity (darkness) in the glaucomatous retina was determined relative to the labeling found in the control retina by image analysis. Ganglion cell density was estimated from radial sections in the parafovea and from retinal whole mounts in the mid-periphery. The number of Müller cells was estimated from vibratome sections immunolabeled by vimentin antibodies in the temporal mid-periphery (about 30 degrees). Glutamine immunoreactivity was localized predominately in ganglion cells and Müller cells. However, the intensity of glutamine immunolabeling was greater in Müller cells of glaucomatous eyes than in control eyes. This increase in glutamine immunolabeling was 25-32% in the temporal mid-periphery and 27-48% in the parafovea. Müller cell number in the glaucomatous eye was similar to that of the control in the temporal mid-periphery. The data in this study indicate that the increase in glutamine in Müller cells is not a consequence of their loss and that Müller cell function in the glutamate-glutamine cycle continues in glaucomatous eyes. These findings are consistent with a previous report that extracellular/vitreal glutamate concentration is elevated in high-tension glaucoma.
  3. Carter-Dawson L, Shen F, Harwerth RS, Smith EL, Crawford MLJ and Chuang A. Glutamine immunoreactivity in Müller cells of monkey eyes with experimental glaucoma. Exp. Eye Res. 66:537, 1998.
  4. Harwerth RS, Carter-Dawson L, Shen F, Smith EL and Crawford MLJ. Ganglion cell losses underlying visual field defects from experimental glaucoma. Invest. Ophthalmol. Vis Sci. 40:2242, 1999.
  5. Shen F, Harwerth RS, Smith EL, Crawford MLJ and Carter-Dawson L. Müller cell changes in monkey eyes with experimental glaucoma (manuscript in review).

 

Faculty Biography

Louvenia Carter-Dawson, Ph.D.
  • Louvenia Carter-Dawson, Ph.D.
    Associate Professor
  • Department of Ophthalmology
  • University of Texas-Houston Medical School
    6431 Fannin, MSB 7.024
    Houston, TX 77030
  • phone: (713) 500-5980
    e-mail: Louvenia.Carter-Dawson@uth.tmc.edu
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