Whole-cell currents activated at nicotinic acetylcholine receptors on ganglion cells isolated from goldfish retina.
We have recorded whole-cell membrane currents in response to exogenously applied acetylcholine (ACh), nicotine, and 1,1 dimethyl-4-phenyl piperazinium iodide on retinal ganglion cells enzymatically dissociated from goldfish retina. Agonist applications induced nicotinic-type responses in a majority of cells when cells were isolated under optimal conditions. Currents were reminiscent of nicotinic-type ganglionic responses. Dose-response measurements of ACh-induced currents indicated an EC50 of 52 microM and a Hill coefficient of 0.6. Currents were selective for Na+ over Cl- and were highly inwardly rectifying. Responses were blocked reversibly by d-tubocurarine, hexamethonium chloride, and N-methyl-D-glucamine. In 50% of the cases, alpha-bungarotoxin reversibly blocked the current induced by ACh application. The blocking action of mecamylamine was irreversible and independent of the presence of agonist but was more effective in the presence of ACh. We conclude that functional nicotinic ACh receptors exist on most goldfish retinal ganglion cells.
Yazejian
B
B
Department of Ophthalmology, Jules Stein Eye Institute, UCLA School of Medicine 90024-1770.
Fain
G L
GL
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D004246:Dimethylphenylpiperazinium Iodide / Q000494:pharmacology; D004594:Electrophysiology; D006054:Goldfish; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009538:Nicotine / Q000494:pharmacology; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000502:physiology*; D012165:Retinal Ganglion Cells / Q000187:drug effects / Q000502:physiology*
D011978:Receptors, Nicotinic; D004246:Dimethylphenylpiperazinium Iodide; D009538:Nicotine; D000109:Acetylcholine