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Neurotransmitter actions on transient amacrine and ganglion cells of the turtle retina

Published online by Cambridge University Press:  03 May 2004

Jozsef Vigh
Affiliation:
Department General Zoology and Comparative Neurobiology, University of Pecs, H7601 Pecs, Hungary Department Ophthalmology, New York University School of Medicine, New York
Paul Witkovsky
Affiliation:
Department Ophthalmology, New York University School of Medicine, New York Department Physiology and Neuroscience, New York University School of Medicine, New York

Abstract

We obtained intracellular recordings from transient, On–Off amacrine and ganglion cells of the turtle retina. We tested the ability of neurotransmitter agonists and antagonists to modify the responses to light stimuli. The metabotropic glutamate agonist, 2-amino-phosphonobutyric acid (APB), selectively blocked On responses, whereas the amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) receptor antagonist, GYKI, blocked both On and Off responses. Although GYKI appeared to block excitation completely, suggesting an absence of N-methyl-d-aspartate (NMDA)-mediated responses, it was found that in the presence of ionotropic gamma-aminobutyric acid (GABA) blockers, the excitatory postsynaptic potential (EPSP) was prolonged. The late component of the EPSP was blocked by the NMDA antagonist, D-2-amino-5-phosphopentanoic acid (D-AP5). Picrotoxin (PTX) and bicuculline (BCC) induced a mean hyperpolarization of −6.4 mV, suggesting a direct effect of GABA on transient amacrine and ganglion cells, since antagonism of a GABA-mediated inhibition of release of glutamate by bipolars would depolarize third-order neurons. The acetylcholine agonist, carbachol, or the nicotinic agonist, epibatidine, depolarized all On–Off neurons. This action was blocked by d-tubocurarine. Cholinergic inputs to On–Off neurons increase their excitability without altering the pattern of light responsiveness.

Type
Research Article
Copyright
2004 Cambridge University Press

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