[Abstract Title]. - Society for Neuroscience

axons at DIV 18-22. Using this system, we examined the effect of several neurotrophic factors
that have been reported previously to promote myelination. Both ciliary neurotrophic factor and
leukemia inhibitor factor markedly promoted OL differentiation and survival but only
moderately increased myelin formation. In contrast, γ-secretase inhibitor DAPT did not promote
OL survival and differentiation, but significantly increased the population of ensheathing OLs
and enhanced myelination in a concentration-dependent manner. Notch signaling has been
implicated in regulating OL development and is subjected to γ-secretase regulation. The Notch
ligand contactin/F3 appears to promote OL differentiation whereas Jagged1 inhibits OL
differentiation. To examine whether DAPT promotes myelination by blocking the Notch
signaling, the effect of soluble contactin1 and Jagged1 was studied. While contactin1
significantly increased the number of internodes, Jagged1 had no effect. Combination of
contactin1 and DAPT resulted in further increases in myelin formation. These data suggest that
modulation of Notch signaling pathways may provide a new strategy for promoting CNS
myelination and myelin repair.
Disclosures: H. Koito, None; J. Li, None.
Poster
241. Glial Neuronal Interactions
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 241.2/F8
Topic: B.11.b. Cell biology and signalling
Support: NS050705
Title: Regulation of connexins in proliferating Schwann cells
Authors: *M. M. FREIDIN, S. ASCHE, C. K. ABRAMS;
Dept Neurol, SUNY Downstate Med. Ctr., Brooklyn, NY
Abstract: Our lab has recently reported that Glial Growth factor II (GGF2), a member of the
neuregulin family of growth factors, increases Schwann Cell (SC) expression of Connexin32
(Cx32) and promotes SC survival, proliferation, and differentiation. Increases in GGF2 and its
receptors (ErbB2 & ErbB3) are associated with SC proliferation during Wallerian degeneration.
In addition, we found proliferating and non-proliferating populations of wild type (WT) SCs
express Cx32, while SCs from Cx32-null (32KO) mice show reduced proliferative response to
Neg1 as compared to WT. GGF2 also increases junctional conductances in WT SCs. Some of
these cell-cell channels are characteristic of Cx32; however, the patterns of coupling are
sufficiently complex and varied to suggest the involvement of additional connexins. Other