Progressive brain damage accelerates axon sprouting in the adult rat.

An entorhinal cortical lesion causes undamaged fibers in the deafferented hippocampus to sprout and form new connections within 4 to 7 days after the lesion was made. When a partial lesion of the entorhinal cortex precedes a second, more complete entorhinal lesion by a few days, the rate of axon sprouting is accelerated so that the response to the second lesion occurs within only 2 days. This priming effect is present within 4 days, lasts for a few weeks, and eventually subsides. This acceleration may explain, in part, the faster recovery and reduced deficits seen in behavioral studies that have followed serial lesion paradigms.