Sayer, et al. (2002). Neurotrophins reduce degeneration of injured ascending sensory and corticospinal motor axons in adult rat spinal cord.

[Wise Young]

• Sayer FT, Oudega M and Hagg T (2002). Neurotrophins reduce degeneration of injured ascending sensory and corticospinal motor axons in adult rat spinal cord. Exp Neurol. 175 (1): 282-96. Summary: Spinal cord regeneration in adult mammals is limited by neurite outgrowth inhibitors and insufficient availability of outgrowth-promoting agents. Formation of degenerative swellings at the proximal ends of severed axons (terminal clubs), which starts early after injury, also may hinder recovery and their rupture may contribute to secondary spinal cord damage. We investigated whether neurotrophins would reduce these degenerative processes. Adult rats received a transection of the dorsal column sensory and corticospinal motor tracts at T9 and anterograde tracing of the axons from the sciatic nerve and motor cortex, respectively. The highest number of terminal clubs was found at 1 day and approximately half remained present until at least 28 days. A single injection immediately after injury of a mixture of nerve growth factor, brain-derived neurotrophic factor and neurotrophin-3 into the lesion site, reduced the number of terminal clubs in the sensory system by approximately half at 1 and 7 days (but not 14) after the lesion. Individual or combinations of two neurotrophins were as effective, suggesting that the neurotrophins protected similar axonal populations. The injected neurotrophins did not affect degeneration of corticospinal motor axons. A 7-day continuous intrathecal infusion of neurotrophin-3 was more effective and also reduced terminal club formation of corticospinal axons by approximately 60%. Spinal tissue loss was not affected by the neurotrophin treatments, suggesting that terminal clubs are not major contributors to the pathogenesis of secondary spinal degeneration during the first two weeks. Thus, neurotrophins can reduce axonal degeneration in the spinal cord after traumatic axonal injury. (c) 2002 Elsevier Science (USA). <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12009779> Kentucky Spinal Cord Injury Research Center, University of Louisville, Kentucky, 40292

[sherry38]

Thank you Dr. Young.
I found this article extremely interesting. A little baffled by the medical terms though http://sci.rutgers.edu/forum/images/smilies/wink.gif *Still a medical term nimrod http://sci.rutgers.edu/forum/images/smilies/wink.gif *
Am I correct that this shows improvement especially in secondary injury, when administered right after injury?
Is this in conjuction with the steriods or separate?
Is it showing re-growth in those terminal clubs?
Woe!

"every man is my superior, that I may learn from him" Plato

[Wise Young]

sherry38, this is actually one of a series of studies that are showing a trend in the field. There is much talk about degeneration of axons after spinal cord injury. For nearly a century, scientists have know that the part of the axon that is still attached to the cell body will die back a short distance from the injury site. These axons show bulbous enlargements at the end and scientists have long assumed that these axons have stopped growing. What the authors report is that when they drip neurotrophins into the areas of the brain that sent the axons, the treatment significant reduced the number of these end bulbs. They thus adopted the more classical view that these end-bulbs are a bad sign and concluded that neurotrophin treatments are good because they reduce the number of end-bulbs. Please note an earlier study by Plunett, et al.(2002) (http://carecure.org/forum/showthread.php?t=36805), reporting that neurotrophins can reverse atrophy of rubrospinal neurons as long as a year after injury. Thus, this is one of several groups that are now beginning to advocate neurotrophin application to the brain. This is of interest because most therapies have been applied to the spinal cord rather than the brain.

Wise.