This thesis addresses the question of how direction selectivity (DS) arises in the mouse retina. DS has long been observed in retinal ganglion cells [barlow1963selective], and more recently confirmed in the starburst amacrine cell [Euler:2002oq]. Upstream retinal bipolar cells, however, have been shown to lack DS [Yonehara:2013hc], indicating that the mechanism that gives rise to DS lies in the inner plexiform layer, where the axons of bipolar cells costratify with amacrine and ganglion cells. We reconstructed a region of the IPL and identified cell types within it. We discovered a novel mechanism which may explain the origin of DS activity in the mammalian retina, which relies on what we call “space-time wiring specificity.” It has been suggested that a DS signal can arise from non-DS excitatory inputs if at least one among spatially segregated inputs transmits its signal with some delay [reichardt1961autocorrelation], which we extend to consider also a difference in the degree to which the signal is sustained. Previously, it has been supposed that this delay occurs within the starburst amacrine cells' dendrites [Hausselt:2007nx]. We hypothesized an alternative, presynaptic mechanism. We observed that different bipolar cell types, which are believed to express different degrees of sustained activity [Baden:2013uq], contact different regions of the starburst amacrine cell dendrite, giving rise to a space-time wiring specifity that should produce a DS signal. We additionally provide a model that predicts the strength of DS as a function of the spatial segregation of inputs and the temporal delay.