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The goal of this study was to evaluate different neurotransmitters and their receptors that might be involved in retinotectal transmission in the goldfish. Sections of tectum were isolated and maintained in vitro while pharmacological agents were administered via the tissue bath. Field potentials were elicited by electrical stimulation of the optic nerve and recorded at 50 micron depth intervals, and profiles of current source densities (CSDs) were computed from the second spatial derivatives of these potentials. The preparations were treated with low [Ca2+]/high [Mg2+] media, various cholinergic agonists and antagonists, eserine, strychnine, or kynurenic acid, via the tissue bath. Prior to treatment, depth profiles of these in vitro field potentials and CSDs closely resembled those previously reported in vivo, including 2 prominent sink-source pairs with their sinks in the superficial optic neuropil, followed by a smaller and more prolonged sink-source pair of opposite polarity. These were rapidly and reversibly eliminated by low [Ca2+]/high [Mg2+] bathing media, and substantially reduced by 0.5 or 1.0 mM kynurenic acid. By contrast, d-tubocurarine (d-TC; up to 0.16 mM) reduced peak response amplitudes by less than 40%, eliminated the third sink-source pair, and more than doubled the duration of decay of sink-source pairs 1 and 2 in a concentration-dependent manner. Strychnine had a similar action to d-TC but was slightly more potent. The time course and amplitudes of responses were not much affected by the following nicotinic agonists or antagonists (concentrations in microM): mecamylamine, 50; dihydro-beta-erythroidine, 50; nicotine, 200; tetramethylammonium, 500; ACh (protected by eserine, 20), 200; alpha-bungarotoxin, 2 microM for 2.5 hr, and 0.4 microM for up to 10.5 hr; and lophotoxin, 32 microM for up to 94 min. Eserine (20 microM) and carbachol (200 microM) increased peak response amplitudes by up to 80% within 5–10 min, and amplitudes remained elevated during 20–33 min of continued treatment. The onset of the effects of d-TC, strychnine, and kynurenic acid began in 5–10 min and was completed in 30 min or less, indicating that test substances could adequately penetrate into the interior of the isolated sections of tectum. The failure of these cholinergic ligands to prevent postsynaptic responses indicates that excitatory retinotectal transmission does not depend on an intact nicotinic (or other cholinergic) system, as previously proposed. The action by kynurenic acid suggests the involvement of an excitatory amino acid neurotransmitter in retinotectal transmission.(ABSTRACT TRUNCATED AT 400 WORDS)

Pharmacology of retinotectal transmission in the goldfish: effects of nicotinic ligands, strychnine, and kynurenic acid