[Abstract Title]. - Society for Neuroscience

interest, since MBP is thought to be synthesized in free polysomes and not in the ER. ER stressrelated
regulation of myelin protein transcription factors and downstream decreased expression
of MBP could help explain myelin loss in certain acquired and heritable white matter disease.
Understanding the effects of ER stress on glial cells could lead to targeted therapeutic
interventions in these disorders.
Disclosures: A. Takanohashi , None; A. Vanderver, None.
Poster
252. Demyelinating Disorders: Mechanisms and Therapeutics II
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 252.2/W26
Topic: C.08.a. Molecular and cellular mechanisms
Support: New Jersey Commission on Spinal Cord Research
New Jersey Commission on Brain Injury Research
Title: Schwann cell proliferation following PNS demyelination: Are they coupled to one
another?
Authors: *D. YANG, H. A. KIM;
Biol. Sci., Rutgers Univ., Newark, NJ
Abstract: Injury to peripheral nerves initiates a sequence of injury responses in the distal
Schwann cells termed Wallerian degeneration: Schwann cell demyelination is followed by
dedifferentiation and proliferation. The nature of the signal that initiates the Schwann cell
response is unknown. Glial growth factor (GGF) is a potent Schwann cell mitogen which
belongs to the neuregulin-1 (Nrg-1) growth factor family. Treatment of myelinating co-culture
with GGF induces demyelination followed by Schwann cell proliferation, indicating the
demyelinating function of the growth factor is coupled to its mitogenic function. To address the
issue, we tested the functions of other Schwann cell mitogens, TGF-b, PDGF, FGF-2 and EGFdomain
of Nrg-1, on initiating demyelination.
These growth factors, when combined with elevated levels of cAMP, have been shown to
stimulate Schwann cell proliferation. We also tested the effect of CRD-Nrg-1, a Nrg-1 isoform
that has been shown to promote myelination.
Under a mitogenic condition, FGF-2 induced demyelination in the co-culture system as seen with
GGF. However, TGF-b and PDGF failed to do so, indicating that the mitogenic function of a
growth factor is not necessarily coupled to demyelination. Interestingly, the EGF-domain of Nrg-