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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Effects of nasal inflammation on the olfactory bulb

Fig. 1

Schematic diagram of the olfactory bulb in response to chronic nasal inflammation. A Chronic nasal inflammation induces atrophy of the olfactory bulb (OB). The superficial OB layers including the olfactory nerve layer (ONL), glomerular layer (GL), and superficial external plexiform layer (sEPL) become thinner in response to nasal inflammation. The deeper layers of the OB including the deep EPL (dEPL), mitral cell layer (MCL), internal plexiform layer (IPL), and granule cell layer (GCL) do not change in thickness in response to nasal inflammation. Orientation of the lateral (L) region of each olfactory bulb is indicated by the arrows. B, C OB neurocircuitry following challenge of chronic nasal inflammation. Multiple anatomical, cellular, and molecular changes take place in the OB following nasal inflammation. Fewer OSN axons are present in the ONL and GL due to their degeneration. This loss of OSN input to the OB is a significant factor in the shrinkage of the glomeruli. The ONL, GL, and sEPL all become significantly thinner. Glial cells such as microglia and astrocytes are more prevalent and begin to activate in these layers in response to chronic inflammation. Various pro- and anti-inflammatory cytokines begin to accumulate in the superficial layers. Fewer dendrodendritic synapses are present in the sEPL. Tufted (T) cell lateral dendrites retract throughout the sEPL and the axon initial segments of T cells become fewer in number and shorter in length, while mitral (M) cells are largely unaffected. Orientation of the lateral (L) region of each olfactory bulb is indicated by the arrows on to the left and right of figure (B) and (C), respectively. G: granule cell

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