Five hundred twenty ganglion cells in an isolated whole-mount preparation of the mouse retina were labeled using the "DiOlistic" method and were classified according to their morphological properties. Tungsten particles coated with a lipophilic dye (Dil) were propelled into the whole-mount retina using a gene gun. When a dye-coated particle contacted the cell membrane, the entire cell was labeled. The ganglion cells were classified into four groups based on their soma size, dendritic field size, and pattern and level of stratification. Broadly monostratified cells were classified into three groups: RGA cells (large soma, large dendritic field), RGB cells (small to medium-sized soma, small to medium-sized dendritic field), and RGc cells (small to medium-sized size soma, medium-sized to large dendritic field). Bistratified cells were classified as RGD. This study represents the most complete morphological classification of mouse retinal ganglion cells available to date and provides a foundation for further understanding of the correlation of physiology and morphology and ganglion cell function with genetically manipulated animals. Optokinetic Nystagmus (OKN) is a type of eye movement thought to minimize retinal image motion. Existing evidence indicate that both types of direction selective ganglion cells (DSGCs) might involve in driving OKN. In this study we attempted to correlate results of behavioral studies with responses of electrophysiological recorded DSGCs. Various reagents known to affect retinal DS were intraocularly injected and the impacts on OKN observed. Intraocular concentration was. estimated for each reagent and used in vitro experiments observing electrophysiological responses of DSGCs to these reagents recorded in whole cell mode. NMDA antagonist AP-7 suppressed responses to a drifting bar of both DSGCs by about 30%, but did not affect the OKN. Intraocular injection of nicotinic ACh receptor antagonist D-tubocurarine completely blocked OKN, and suppressed the responses of ON DSGCs to a drifting bar by 70%, but suppressed the ON-OFF DSGCs' response only by 30%, Intraocular injection of 20 uMNMDA induced nystagmus, same concentration elicits vigorous spiking in ON DSGCs but never on ON-OFF DSGCs. The dose-response curve of NMDA induced nystagmus corresponded to that of the spiking response of the ONDSGCs. These results suggested that activation of the ON DSGCs is sufficient and necessary in driving nystagmus.