Layer I GABAergic inhibitory interneurons, which are believed to mediate feedforward inhibition by receiving direct mitral/tufted cell input (Stokes and Isaacson, 2010) are more broadly tuned to odors than pyramidal cells (Miyamichi et al., 2011 and Poo and Isaacson, 2009). These interneurons are hypothesized to have either a lower threshold or receive greater convergence of mitral/tufted

cell inputs than pyramidal cells (Poo and Isaacson, 2009). Thus, while pyramidal cells express excitatory responses to relatively few odors in a test stimulus set, the same cells show broadly tuned inhibitory responses. Thus, as in other systems, inhibition can play an important role in shaping stimulus receptive fields. Interneurons in layers II and III are more typically targets of intracortical association fiber inputs or input from nonpiriform sources. These Talazoparib supplier GABAergic interneurons tend to terminate on pyramidal cell proximal dendrites, soma, or axon initial segments and can be highly effective at blocking pyramidal cell output either via shunting inhibition or action potential blockade (Luna and

Schoppa, 2008). GABAergic interneurons in check details each layer also show a dichotomy in their response to excitatory synaptic input. A subset of interneurons in each layer show strong initial response to excitatory input evoking spiking output, while another subset show weaker initial responses but facilitation over repeated stimulation (Suzuki and Bekkers, 2010a). Suzuki and Bekkers suggest these differences in synaptic physiology could allow a temporal segregation of activity, with different interneurons producing output at different phases of the respiratory cycle. The respiratory cycle is a strong source of oscillations throughout the olfactory pathway; however, several other spontaneous and induced oscillations are also prominent. For example, beta (15–35 Hz) and gamma (35–90 Hz) frequency oscillations can be robustly

evoked in the piriform cortex, generally in phase with the 2–4 Hz respiratory cycle. Current source density analyses suggest that these higher frequency oscillations derive from the cyclical afferent-association fiber activity loop, shaped by synaptic inhibition (Ketchum and Haberly, 1993). More recently, in vivo whole-cell recordings from Parvulin piriform cortex pyramidal cells supported this by showing that pyramidal cell spiking was phase locked to beta frequency oscillations and that this phase locking was partially governed by synaptic inhibition (Poo and Isaacson, 2009). As mentioned above, precise timing of pyramidal cell activity can reinforce temporal convergence of afferent synaptic excitation driven by the current odor input with association fiber synaptic excitation which reflects both ongoing sensory input and previous experience (due to experience-dependent synaptic potentiation during past odor stimuli).