Depolarization elicits,while hyperpolarization blocks uptake of endogenous glutamate by retinal horizontal cells of the turtle |
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Authors: | Michael Schütte Etha Schlemermeyer |
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Institution: | (1) Department of Ophthalmology, New York University Medical Center, 550 First Avenue, 10016 New York, NY, USA;(2) Department of Biology, Hunter College of the City University of New York, 695 Park Avenue, 10021 New York, NY, USA;(3) Department of Psychology, Queens College of CUNY, 11367 Flushing, NY, USA |
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Abstract: | We have employed an immunoreaction against glutamate to qualitatively demonstrate varying levels of glutamate in retinal horizontal cells of the turtle. Glutamate-like immunoreactivity (GLI) in horizontal cells could be demonstrated after glutamate decarboxylase was inhibited by aminooxy acetic acid (AOAA) and its degradation to GABA was blocked. Depolarization of horizontal cells by kainic acid (KA) induces strong glutamate immunoreactivity in these cells, whereas hyperpolarization by 2,3-cis piperidine dicarboxylate (PDA) abolishes glutamate-like immunoreactivity in horizontal cells. When glutamate release from cones and bipolar cells is blocked in the absence of calcium, or when glutamate uptake is blocked by DL-threo -hydroxy aspartate, KA/AOAA treatment of the retina does not induce GLI in horizontal cells. Our data show that horizontal cells are capable of taking up glutamate from the endogenous retinal pool in an activity dependent way. Our interpretation of these findings is that retinal horizontal cells are capable of regulating glutamate levels in the extracellular space of the cone pedicle complex by an activity-dependent uptake system. We suggest that inhibition of glutamate uptake upon hyperpolarization rather than inhibition of GABA release may evoke the antagonistic surround response of retinal bipolar cells. |
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