[Abstract Title]. - Society for Neuroscience

in the anti-inflammatory cytokines. Together these data suggest the BM-hMSCs represent a
viable option for therapeutic approaches.
Disclosures: L. Bai, None; R.H. Miller , None.
Poster
251. Demyelinating Disorders: Animal Models and Human Studies I
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 251.29/W22
Topic: C.08.b. Animal models
Support: Myelin Repair Foundation
Title: Progression of functional recovery in lysolecithin demyelinating models in adult rats
Authors: *Y.-H. HSIEH 1 , R. MILLER 1 , C. WILSON 2 ;
1 Dept Neurosci., 2 Dept Pediatrics, Case Western Res. Univ., Cleveland, OH
Abstract: The failure of remyelination can lead to pathophysiologic impairment that mimics
Multiple Sclerosis including axonal damage, astrocytosis, and prominent inflammatory infiltrate.
However, there is little data on functional changes over time in central nervous system neural
circuits and the precise contribution of demyelination/remyelination to functional conduction in
white matter axons is not clearly defined. Models of demyelinating spinal cord lesions involving
the injection of lysolecithin (LPC) have been developed to better understand the biology of
remyelination and this model allows quantification of neural pathway recovery using
electrophysiological methods. We hypothesize that functional recovery parallels
histological/morphologic markers of full remyelination. To test our hypothesis, we use an in vivo
adult rat model (Sprague Dawley, 325-350 g) to evaluate both functional deficits in neural
transmission along these tracts as well as time course and degree of recovery following LPC
lesions. We electrically stimulate (L1) and record (C3) in anatomically identified axonal tracts
containing LPC lesions (T12) in the dorsal column of the spinal cord to examine the compound
evoked potential and conduction velocity. Black-Gold staining was utilized to morphologically
identify the extent of demyelination/remyelination. Our preliminary functional data show that
despite remyelination at 14 days post injection (dpi), incomplete recovery of signal transmission
persists (10% when comparing the area of the evoked compound potential from the lesion to the
non-lesioned control side). By 21 dpi, a 40% recovery is observed. Full recovery is observed by
28 dpi. These results suggest that histological markers of remyelination do not correlate with
functional recovery of transmission.