, 2007). We found that inhibition in MCs has a robust fast component, followed by delayed synaptic events that last longer than 100 ms.

The fast component of inhibition accounted for only about 20% of the total charge, but because of its synchronous nature can lead to strong suppression of activity. It has been known this website for some time that elementary inhibitory events from GCs evoked by MC activation continue to occur for hundreds of milliseconds (Isaacson and Strowbridge, 1998; Schoppa et al., 1998). Here, we find that similar delayed events can occur after activation of GCs through AON axons, but the time constant of these events is shorter than that reported for dendrodendritic inhibition evoked by depolarizing MCs (Isaacson and Strowbridge, 1998; Schoppa et al., 1998). This difference could be due to the manner in which GCs are activated: cortical axons appear to target proximal dendrites of GCs and evoke larger quantal Dolutegravir mouse events with faster kinetics, whereas MC synapses are made on distal dendrites, have lower amplitudes and slower kinetics. These differences could lead to more gradual depolarization of GCs when MCs are active, allowing the A-type potassium currents to delay spiking in GCs. We found that activation

of AON synapses often results in immediate spiking of GCs within a few milliseconds, perhaps due to the larger amplitude, faster synaptic inputs. Rapid inhibition in MCs triggered by activation of AON axons appears to be well-placed to impose timing constraints on MC spiking. Because MC spike timing has clearly been shown to be an important part of odor information Amisulpride leaving the OB (Cury and Uchida, 2010; Dhawale et al.,

2010; Shusterman et al., 2011), the AON is in a key position to influence it. Although anatomical studies have identified glomerular innervation of AON axons, no functional studies have been undertaken until now due to the difficulty in selectively stimulating AON axons. Here, by optical stimulation of identified AON axons, we have identified several target neurons in the glomerular layer including ETCs, PGCs, and SACs. Although AON axons excited ETCs, they rarely evoked LLDs, which lead to glomerulus-wide excitation and large depolarizations in MCs (Gire et al., 2012). The direct excitation of glomerular interneurons by AON, combined with the absence of glomerular LLDs, results in a net inhibition to MCs. In fact, our experiments suggest that more than 30% of the transient inhibition on MCs arises from the glomerular layer. Remarkably, cortical feedback is capable of influencing information flow at the very first synaptic processing stage in the OB. Glomerular inhibition can be effective in shunting out sensory input because MCs may rely on input from ET cells more than direct sensory nerve input (Najac et al., 2011; Gire et al., 2012).