The conspicuous hairpin loop made by a primary neurite
close to the SFGS ( Figure S2D3) suggests that repulsion due to molecular interaction between pre- and postsynaptic selleck inhibitor structures could be responsible for this avoidance. Several mechanistic models have been proposed that can explain DS (Barlow and Levick, 1965; Adelson and Bergen, 1985; Priebe and Ferster, 2005; Borst and Euler, 2011; Vaney et al., 2012). These differ in particular in two aspects: one is the degree in which excitatory inputs are directionally tuned and thus control the directional tuning of the postsynaptic cell. Another is the role of inhibitory input tuning in the same or opposite direction (preferred- versus null-direction inhibition). In the tectal DS neurons described here, the spike output tuning curve was aligned with the tuning of excitatory inputs. This suggests that presynaptic excitatory DS neurons determine the PD of these cell types. In addition, a spike threshold may suppress nonspecific excitatory inputs and contribute to sharpening the directional response in the presence of
noise (Priebe and Ferster, 2005). Furthermore, inhibitory inputs were tuned to the null direction in most, but not all, of the morphologically identified neurons described here. Recently, null-direction inhibition was suggested to underlie directional Sorafenib datasheet tuning in randomly selected almost tectal neurons of undescribed morphology (Grama and Engert, 2012). Here, using multiphoton targeted patch-clamp recordings, we identified morphologically distinct inhibitory type 1 and type 2 cells, which are good candidates for providing the source of such DS inhibition. It should be noted, however, that the pronounced DS of excitatory inputs in these cell types argues against the notion that null-direction inhibition critically
determines the emergence of DS spike output in tectal neurons in general. In addition to shaping the output tuning curve, inhibition may also be important in controlling the timing of spike output. We observed that firing rate peaked at times when EPSCs reached their maximum during bar presentation but dropped when EPSCs and inhibitory postsynaptic currents (IPSCs) coincided in time, both in preferred and nonpreferred directions. Also, short firing rate bursts could be seen after decay of inhibitory currents in some cases, consistent with a postinhibitory rebound mechanism for spiking. More experiments are necessary to determine how the timing of excitation and inhibition shapes the temporal code of tectal motion processing. A parsimonious explanation for how DS emerges in type 1 and type 2 neurons builds on the finding of lamina-specific targeting of dendritic/axonal compartments together with directionally tuned synaptic excitation.
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