To test this idea, we performed chronic imaging of the activity of olfactory sensory neuron synapses in the glomerular layer using OMP-synapto-pHluorin mice (Bozza et al., 2004), in which all OSNs express synapto-pHluorin, a reporter of neurotransmitter release (Figure 5A). We imaged OSN transmission with the same 1 week protocol

used for studying mitral cell plasticity (Figure 5B). Each odor activated a unique ensemble of glomeruli (Figure 5C), consistent with previous reports (Belluscio and Katz, 2001; Bozza et al., 2004; Igarashi and Mori, 2005; Johnson et al., 2005; Onoda, 1992; Rubin and Katz, 1999; Stewart et al., 1979; Wachowiak and Cohen, 2001; Xu et al., 2000, 2003; Yang et al., 1998). In stark contrast to mitral cell activity, presynaptic input to the bulb remained stable over the course of the experiment for both experienced and less-experienced odors (Figures 5C–5E). This is not due Selleckchem Cabozantinib to saturation Docetaxel clinical trial of the synapto-pHluorin signal, since higher odor concentrations triggered stronger responses (Figure S1). In addition, mitral cell glomerular GCaMP3 responses, which reflect a combination of local synaptic excitation of mitral cell dendrites by OSN input and backpropagating action potentials, show only a modest reduction during the same odor experience protocol (Figure S8). Thus, these results indicate that experience-dependent plasticity of mitral cell activity

must be generated by changes downstream of sensory neuron input to the bulb. Does the response plasticity of mitral cells Cell press to experienced odors happen only once in the lifetime of an animal and leave a permanent “imprint” of odor experience or is this a dynamic process that shapes odor representations throughout life? To distinguish these possibilities, we examined the persistence of the effect of odor experience by testing odor responses at various time points after home cage rearing without additional odor applications (Figure 6A, “recovery”). Seven days of home cage rearing led to a partial recovery of mitral cell responses. Further recovery was seen after 3 more weeks,

and responses recovered completely after 2 months (Figures 6B and 6C). Odor representations after full recovery resembled those on the initial day (day A1, Figure 6D). Thus, the effect of odor experience on mitral cell responses persists for weeks but not months. After full recovery of the plasticity to odor set A, we repeated the 1 week odor experience protocol, this time using odor set B for the experienced odors (Figure 6A, “odor set B experience,” n = 3 mice, 132 mitral cells). After 1 week of daily experience with odor set B, the responses of mitral cells were selectively reduced to set B odors while their responses to set A odors were maintained (Figures 6B and 6C). Furthermore, the magnitude and time course of the modulation of the population response were virtually identical for the two separate bouts of odor experience (Figure 6C).