Synapse formation after injury in the adult rat brain: failure of fimbrial axons to reinnervate the bed nucleus of the stria terminalis.
Selectivity in the reinnervation of denervated postsynaptic sites in the adult rat septal nuclei has been studied by both light and electron microscopic degeneration techniques after lesions of the fimbria and stria terminalis. In the mid-rostrocaudal septum the ventral border of the lateral septal nucleus is coextensive with the dorsal border of the strial bed nucleus. In the normal rat, fimbrial axons establish synapses throughout the lateral septal nucleus of the same side, and also in the dorsal part of the lateral septal nucleus on the opposite side. The stria terminalis establishes synapses in the ipsilateral but not in the contralateral bed nucleus at this level. Both the fimbria and the stria terminalis were completely severed on the left side, and after adequate survival for the removal of all degeneration, the distribution of the remaining fimbria was plotted. Interesting changes were found on the side contralateral to the second lesion, where the fimbria both increases the number of its synaptic terminals within its proper contralateral territory (the dorsal part of the lateral septal nucleus) and also extends its distribution into the ventral part of the lateral septal nucleus--the territory normally reserved for the ipsilateral fimbria. Although completely surrounding the strial bed nucleus, fimbrial axons fail to invade the bed nucleus, and fimbrial terminals are therefore unable to reinnervate denervated strial postsynaptic sites. Since there are no obvious structural barriers between the neuropil of the lateral septal nucleus and that of the strial bed nucleus it is suggested that this failure is most likely to be due either to some biochemical incompatibility between fimbrial axons and strial postsynaptic sites, or to the fact that the fimbrial axons are denied access because some other (unidentified) axonal system forms new presynaptic terminals which effectively pre-empt the sites in the strial bed nucleus.
D000818:Animals; D001369:Axons / Q000502:physiology* / Q000648:ultrastructure; D001921:Brain / Q000503:physiopathology*; D001930:Brain Injuries / Q000503:physiopathology*; D005260:Female; D008854:Microscopy, Electron; D009416:Nerve Regeneration; D051381:Rats; D013569:Synapses / Q000502:physiology* / Q000648:ultrastructure