, 1992). That they innervate the sSC at all is perplexing, because by virtue of their greater synaptic distance from the retina, cortical action potentials should Selleck Pifithrin �� arrive in sSC long after

the direct retinal input has reached the colliculus. Such assumptions suggest a reduced ability of cortical inputs to fire sSC cells, which should lead to depression of corticocollicular inputs. The present data suggest several ways that the brain solves this problem. First, even before EO, cortical axons target regions of DOV cell bodies proximal to the spike initiating zone (Figure 3) and later concentrate on proximal dendrites where they are located in adulthood (Figure 2). This is expected to maximize their depolarization of DOV neurons, which have axons originating ventrally from the soma (Bekkers and Stevens, 1996 and Spruston, 2008). Indeed, we found cortex to be an effective driver of collicular neuronal spiking

as early as 1 day after EO in the deep SGS where DOV neurons are located. Selleckchem Wortmannin Targeting of proximal locations may be a strategy that is widely used in the developing CNS to aid synaptogenesis (Hashimoto et al., 2009). How proximal regions are targeted is uncertain. Some data suggest a laminar selectivity by genetically specified retinal ganglion cell axons within the sSC (Huberman et al., 2008b and Siegert et al., 2009), and DOV neurons sit at the level of cortical axon ingrowth, but this does not prove that the laminar ingrowth or target neurons are prespecified. Because VC axons initially support fewer synapses compared to the preestablished retinal projection, this could

render them more powerful competitors for the previously retina occupied dendritic sites (Figure 3). Support for such a mechanism has been obtained during elimination of competing motor Monoiodotyrosine neuron axons on young muscle fibers (Kasthuri and Lichtman, 2003). Our data suggests a second reason why later arising VC synapses can form stable sSC contacts. Specifically, during pattern vision after EO, we find a rapid flow of excitation through the thalamocortical pathway. Despite a direct retinal input to sSC, peak cortical spiking in L5a precedes the collicular response (Figure 7 and Figure 8). Thus, the ability of cortical neurons to drive collicular neurons with a short (<10 ms) latency could facilitate cortical synapse stabilization through a spike timing dependent mechanism (Froemke et al., 2005, Kobayashi and Poo, 2004 and Zhang et al., 1998). The decreased and sluggish drive of SC units we observed after cortical suppression is somewhat at odds with recent single unit observations in anesthetized adult rodents (Wang et al., 2010). Differences in age and anesthesia will surely contribute to the observed differences, particularly in light of the delayed development of inhibition in the SC (Shi et al., 1997).