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.
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D001369:Axons / Q000502:physiology; D001930:Brain Injuries / Q000473:pathology / Q000503:physiopathology*; D006624:Hippocampus / Q000293:injuries* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009416:Nerve Regeneration; D051381:Rats; D013997:Time Factors
D000110:Acetylcholinesterase