Bipolar cells contribute to nonlinear spatial summation in the brisk-transient (Y) ganglion cell in mammalian retina

The receptive field of the Y-ganglion cell comprises two excitatory mechani sms: one integrates linearly over a narrow field, and the other integrates nonlinearly over a wide field. The linear mechanism has been attributed to input from bipolar cells, and the nonlinear mechanism has been attributed t o input from a class of amacrine cells whose nonlinear "subunits" extend ac ross the linear receptive field and beyond. However, the central component of the nonlinear mechanism could in theory be driven by bipolar input if th at input were rectified. Recording intracellularly from the Y-cell in guine a pig retina, we blocked the peripheral component of the nonlinear mechanis m with tetrodotoxin and found the remaining nonlinear receptive field to be precisely co-spatial with the central component of the linear receptive fi eld. Both linear and nonlinear mechanisms were caused by an excitatory post synaptic potential that reversed near 0 mV. The nonlinear mechanism depende d neither on acetylcholine nor on feedback involving GABA or glycine. Thus the central components of the ganglion cell's linear and nonlinear mechanis ms are apparently driven by synapses from the same rectifying bipolar cell.