Postsynaptic responses of horizontal cells in the tiger salamander retina are mediated by AMPA-preferring receptors.
The postsynaptic responses of sign-preserving second-order retinal neurons (horizontal cells (HCs) and off-bipolar cells) are mediated by CNQX-sensitive AMPA/KA glutamate receptors. In this study we used receptor-specific allosteric regulators of desensitization and selected antagonists to determine the glutamate receptor subtypes in tiger salamander horizontal cells. Two approaches were employed in this study. The first was to measure postsynaptic currents induced by exogenously applied glutamate under voltage clamp conditions in living retinal slices; and the second was to record voltage responses controlled by endogenous glutamate released from photoreceptors in whole retinas. Application of 100 microM cyclothiazide (a specific AMPA receptor desensitization blocker) enhanced the glutamate-induced current by about 5 fold. In contrast, 300 microgram ml-1 Co nA (a specific kainate receptor desensitization blocker), had no effect. GYKI 52466 (a specific AMPA receptor antagonist) at 30 microM almost completely suppressed the glutamate-induced inward current in HCs. Cyclothiazide at 100 microM depolarized the HC dark membrane potential by about 5 mV and reduced the amplitudes of the voltage responses to dim lights, but enhanced the voltage responses to bright lights. Cyclothiazide had no effect on either the dark potential or the light responses of rods and cones. Con A at 300 microgram ml-1 had no effect on either the dark potential or the light responses of the HC. GYKI 52466 (30 microM) hyperpolarized the HC dark membrane potential by about 55 mV and almost completely suppressed the light responses. We conclude from these results that the postsynaptic glutamate- and light-induced responses in the tiger salamander retinal horizontal cells are mediated by AMPA-preferring, and not kainate-preferring glutamate receptors. The functional roles of AMPA receptors and their desensitization kinetics in visual information processing are discussed.
Yang
J H
JH
Cullen Eye Institute, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Maple
B
B
Gao
F
F
Maguire
G
G
Wu
S M
SM
D000557:Ambystoma / Q000502:physiology*; D000818:Animals; D014151:Anti-Anxiety Agents; D000959:Antihypertensive Agents / Q000494:pharmacology; D001569:Benzodiazepines / Q000494:pharmacology; D001581:Benzothiadiazines / Q000494:pharmacology; D003208:Concanavalin A; D003623:Dark Adaptation / Q000502:physiology; D004594:Electrophysiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005456:Fluorescent Dyes; D018698:Glutamic Acid / Q000494:pharmacology; D007546:Isoquinolines; D008564:Membrane Potentials / Q000187:drug effects; D018408:Patch-Clamp Techniques; D010775:Photic Stimulation; D010786:Photoreceptor Cells / Q000737:chemistry* / Q000502:physiology; D018091:Receptors, AMPA / Q000032:analysis*; D013569:Synapses / Q000737:chemistry* / Q000187:drug effects / Q000502:physiology
D014151:Anti-Anxiety Agents; D000959:Antihypertensive Agents; D001581:Benzothiadiazines; D018691:Excitatory Amino Acid Antagonists; D005456:Fluorescent Dyes; D007546:Isoquinolines; D018091:Receptors, AMPA; C061950:GYKI 52466; D003208:Concanavalin A; D001569:Benzodiazepines; D018698:Glutamic Acid; C017475:lucifer yellow; C004639:cyclothiazide