[Abstract Title]. - Society for Neuroscience

ONL of the olfactory bulb in CNPase transgenic mice. Moreover, in culture the OECs maintain
strong eGFP expression, but also show intense immunoreactivity for CNPase. Thus, while OECs
do not normally form myelin on the fine calibre olfactory nerve axons, their upregulation of
CNPase in culture is commensurate with reports that transplantation of cultured OECs can form
myelin when transplanted into demyelinated spinal cord.
Disclosures: C. Radtke, None; K.L. Lankford, None; M. Sasaki, None; V. Gallo, None; J.D.
Kocsis, None.
Poster
252. Demyelinating Disorders: Mechanisms and Therapeutics II
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 252.5/W29
Topic: C.08.a. Molecular and cellular mechanisms
Support: Nancy Davis MS Center Without Walls
Medical Research Service
Department of Veterans Administration
Medical Rehabilitation Research Service
Title: Sodium channel Nav1.6 contributes to macrophage function
Authors: *P. ZHAO 1,2 , J. BLACK 1,2 , S. WAXMAN 1,2 ;
1 Dept Neurol, Yale Univ. Med. Sch., West Haven, CT; 2 Rehabil. Res. Ctr., Vetarans Affairs
Connecticut Healthcare Syst., West Haven, CT
Abstract: Voltage-gated sodium channels are expressed in neurons where they are responsible
for the action potential genesis and conduction. Sodium channels are also expressed in nonexcitable
cells, including glia, immune cells and keratinocytes, but the functional roles of sodium
channels in these cells are not well-understood. As part of studies to determine the contribution
of macrophages to the pathogenesis of inflammatory/demyelinating disorders, we have examined
the expression of sodium channels in macrophages and the contribution of sodium channels to
macrophage functions. Following sciatic nerve crush in adult Sprague-Dawley rats, we observed
the recruitment of large numbers of activated macrophages into the degenerating nerve. In
immunocytochemical studies, sodium channel Nav1.6, but not Nav1.5, was robustly expressed in
these macrophages, and was co-localized with the plasma membrane markers Na/K-ATPase and