This is Alison's paper. Cortical feedback to bulb may be like cortex to thalamus. Express ChR2 in olfactory pyramidal cells. Opening paragraph is even about the oddity that olfactory cortex does not have a thalamus, and the bulb may be playing this role.
IPSCs in MT cells when ChR2 axons stimulated. Disynaptic inhibition mediated by AMPARs. NMDA blockers have no effects. No conventional fast excitatory synatpic responses from cortical to mitral (i.e. driving synapses). However, some small inward currents were observed, blocked by NBQX (AMPAR antagonist), but slow and not responsive to changes in holding potential. Also observed in cells in which the primary apical dendrite was severed. These sound like modulatory feedback inputs, but surprising that they go away even when apical tuft is severed--it seems like most feedback inputs go through apical tuft.
Cortical feedback directly excites GCs, which inhibit MTs. Cortex also drives feed-forward inhibition onto GCs. Net effect on a particular GC could be excitatory or inhibitory. Meditated by deep short axon cells (dSACs). dSACs receive higher convergence of cortical feedback projections, but their numbers are lower.
A similar arrangement of cortical feedback projects to neurons near/in the bulb. Cortical feedback mainly drives inhibitory neurons, and avoids the excitatory cells. E summarizes nicely:
In vivo, ramp LED, allows sustained "self-organized" cortical activity. Gamma ensues, spikes coherent with gamma. Odors produce both gamma and beta. Light + Odors abolishes beta, more spiking in cortex ("layer 2/3"). Cortical activation also drove gamma in bulb.
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