Location: 395 Neuroscience 2012, SfN’s 42nd annual meeting, is scheduled for Oct. 13 -17 in New Orleans at the Ernest N. Morial Convention Center.
Presentation time: Monday, Oct 15, 2012, 9:00 AM – 9:15 AM
Authors: *D. JIN, F. SUN, Z. HE;
Harvard Med. School, Children’s Hosp. Boston, Boston, MA
Abstract: Compensatory sprouting of spared axons has been proposed as
an important structural reorganization mechanism of functional recovery after spinal cord injury, stroke and other types of CNS damages. However, very little is known about how axonal spouting responses are initiated and regulated. Here by using a unilateral pyramidotomy model in which one side of corticospinal tract (CST) axons are transected at the medullary pyramid, we found that deletion of SOCS3, a negative regulator of JAK/STAT pathway, in the cortical neurons promote compensatory sprouting of uninjured CST axons. Further, after this injury CNTF expression is significantly up-regulated in the denervated spinal cord, suggesting that denervation might be an important trigger for cytokine expression and subsequent sprouting responses. Finally, we demonstrated that co-deletion of SOCS3 and PTEN, a negative regulator of the mTOR pathway as well as the intrinsic growth ability of corticospinal neurons, results in further enhanced CST sprouting, suggesting that a combination of SOCS3-dependent extrinsic and PTEN-dependent intrinsic mechanisms is involved in regulating axonal sprouting responses.
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