These data suggest
that retinotopically organized projections from V1 to RL are a determinant of visual responsiveness of RL and hence also of its multimodal character. We made four main findings concerning MI in the mouse visuotactile area RL. (1) ME is more pronounced at the level of spike outputs compared to synaptic inputs; (2) ME is pronounced in supragranular pyramids but scarce among the deep infragranular pyramids and in the main interneuron population—Pv-INs; (3) the scarce ME of Pv-INs permits ME in neighboring pyramids; (4) there is a precise spatial distribution of uni- and bimodal cells at the microscale level. Whole-cell recordings combined with anatomical tracings suggest that RL neurons receive tactile and visual synaptic inputs from S1 and V1, respectively. However, fewer neurons in RL were bimodal al the level of APs than PSPs, and ME was stronger Angiogenesis inhibitor for APs compared to PSPs. This difference is presumably due to the nonlinear threshold mechanism underlying AP generation (see also Allman and Meredith, 2007 and Schroeder and Foxe, 2002). The same threshold mechanism may account for the sublinear summation of PSPs on one hand, and for the (supra)linear summation of APs on the other hand. The multisensory synaptic integration we observed in RL differs from the integration of two different unisensory stimuli in primary cortices. In
primary cortices concurrent presentation of two unisensory stimuli typically suppresses responses, both in S1 ( Higley and Contreras, 2005) selleck kinase inhibitor and V1 ( Priebe and Ferster, 2006),
whereas in RL the interaction was largely additive. Interestingly, a similar difference between unimodal integration (suppression) and bimodal integration (enhancement) has been described in the cat colliculus ( Alvarado et al., 2007). It would be interesting to investigate whether different cellular circuitries are responsible for these distinct computations. While bimodal cells were more abundant in layer 5 compared to layer 2/3, ME was scarce in layer 5 pyramids, already for synaptic inputs. Resminostat However, layer 5 is innervated by layer 2/3 neurons (Thomson and Bannister, 1998), and ME was common in the AP output of layer 2/3 pyramids. Why then do the two cortical layers have different ME, given this connection? A number of mechanisms can be hypothesized. First, many layer 5 cells do not receive inputs from layer 2/3 (Thomson and Bannister, 1998) but instead receive inputs from the thalamus (Ferster and Lindström, 1983) and layer 4 (Feldmeyer et al., 2005). Second, temporal integration properties in the cortex are layer specific. For example, the lower expression of HCN channels in layer 2/3 compared with layer 5 pyramids (Spruston, 2008) could enable stronger ME in layer 2/3, because HCN currents reduce temporal integration (Williams and Stuart, 2000).