The re-innervation of olfactory glomeruli following transection of primary olfactory axons in the central or peripheral nervous system.

The re-innervation of the olfactory bulb has been studied in rats in which the primary afferent axons were transected either in the peripheral nervous system, on the intracranial side of the cribriform plate, or in the central nervous system, in the nerve fibre layer of the bulb. Both procedures resulted in denervation of glomeruli on the dorsal surface of the olfactory bulb. Re-innervation of these glomeruli was first seen approximately three weeks after operation and was largely completed by the sixth week, irrespective of the site of the lesion. The similarity of the timing of re-innervation following the two procedures indicates that the cut fibres did not regenerate from their sites of transection. It is much more probable that the re-innervation axons were those of neurons newly generated in the olfactory epithelium. This view is supported by the results of other investigations, in which retrograde degeneration and subsequent replacement of the neurons have been found to follow transection of the olfactory nerves. After transection of the olfactory nerves, the new axons entering the bulb grew through the site of the lesion, across the interface between peripheral and central nervous tissue, through the nerve fibre layer and into the glomeruli. Thus, they followed the same course as normally growing primary olfactory axons. After the afferent fibres had been cut within the olfactory bulb, the site of transection was transformed into a scar composed largely of astrocytes. No olfactory axons grew through the scar and none passed beneath it in the deeper layers of the bulb. However, by tracing the anterograde axonal transport of horseradish peroxidase, it has been shown that axons immediately rostral to the lesion terminated in the re-innervated glomeruli. These denervated glomeruli were, therefore, probably re-innervated by axons that grew through the intact central nervous tissue of the nerve fibre layer on either side of the lesion.