NEURONAL NICOTINIC ACETYLCHOLINE-RECEPTORS OF GANGLION-CELLS IN THE CAT RETINA

Ganglion cells, retrogradely labeled with DiI, were dissociated from the cat retina. Under the whole-cell clamp mode using a patch pipette, ACh induced a transient current (I-ACh) in all cells tested. The soma diameter of ACh-responsive cells distributed from 11 to 23 mu m, indicating that the preparation included Y, X, and W cells. I-ACh was inward rectifying. The reversal potential of I-ACh was close to the zero-current potential predicted from the intra- and extracellular monovalent cation concentrations by the Goldman-Hodgkin-Katz equation. The concentration-response curve gave a Hill coefficient of 0.89 and an EC(50) of 3.2 X 10(-5) M. Nicotine (10(-4) M) induced a transient current, while muscarine (10(-4) M) was ineffective. The nicotinic antagonist, hexamethonium, reduced the amplitude of I-ACh in a concentration-dependent manner with an IC50 of 1.3 X 10(-6) M. The muscarinic antagonist, atropine, showed a concentration-dependent reduction in the amplitude of I-ACh With an IC50 of 4.4 X 10(-6) M. The amplitude of I-ACh was dependent on the extracellular Ca2+ concentration ([Ca2+](o)); small at low [Ca2+](o) and large at high [Ca2+](o). The time course of desensitization was also dependent on [Ca2+](o); fast at low [Ca2+](o) and slow at high [Ca2+](o). The replacement of extracellular Ca2+ to Sr2+ increased the amplitude of I-ACh, but replacement to other divalent cations reduced it. The results indicate the presence of functional neuronal nicotinic ACh receptors in Y, X, and W cells.