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Light‐induced changes in glutamate release from isolated rat retina is regulated by cyclic guanosine monophosphate
Author(s) -
Barabás Péter,
Kovács Ilona,
Kovács Richárd,
Pálhalmi János,
Kardos Julianna,
Schousboe Arne
Publication year - 2001
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.10117
Subject(s) - zaprinast , glutamate receptor , cyclic guanosine monophosphate , guanosine , retina , biophysics , phosphodiesterase , medicine , endocrinology , chemistry , phosphodiesterase inhibitor , biology , biochemistry , enzyme , neuroscience , receptor , nitric oxide
Abstract Isolated rat retina was preloaded with [ 14 C]glutamate and subsequently superfused to follow release of glutamate (Glu). After 20 min of superfusion in the dark, exposure of the [ 14 C]Glu preloaded rat retina to a single train of white light pulses reduced Glu efflux significantly in the absence as well as in the presence of low (4 μM) and high (0.5 mM) concentrations of the Glu uptake inhibitor trans ‐L‐pyrrolidine‐2,4‐dicarboxylate ( t ‐PDC). The dark–light response was the highest in the presence of 4 μM t ‐PDC by establishing a plateau at 75% ± 7% of the tonic Glu release in the dark (100%). Displaying transient to saturating responses with increasing relative luminance, time series of four trains of white light pulses arrived at a plateau of 85% ± 10%. The cyclic guanosine monophosphate (cGMP) phosphodiesterase inhibitor Zaprinast (200 μM) antagonized the effect of the light series, leading to a plateau of 115% ± 9%. Exposure of the retina to the guanylyl cyclase inhibitor LY83583 (30 and 100 μM) showed fast, transient responses characterized by peaks at 90% ± 1% and 80% ± 3%, respectively. © 2002 Wiley‐Liss, Inc.