Neuroscience 2003 Abstract
| Presentation Number: | 214.7 |
|---|---|
| Abstract Title: | The N-type calcium channel antagonists E2050 and ER-129002-02 ameliorate experimental autoimmune encephalomyelitis (EAE). |
| Authors: |
Smith, T.*1
; Groom, A.1
; Rivers, L.1
; Barden, L.1
; Yamauchi, T.2
; Niidome, T.2
; Iimura, Y.1
; Nishizawa, Y.1
; Yamanishi, Y.2
1Eisai London Res. Lab. Ltd., Univ. Col. London, London, United Kingdom 2Japan, Bernard Katz Bldg, Gower St., WC1E 6BT, |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Demyelinating Disorders |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Neurodegenerative Disorders<br />-- Other |
| Session: |
214. Demyelinating Disorders: Mechanisms of Disease--EAE & PNS Poster |
| Presentation Time: | Sunday, November 9, 2003 10:00 AM-11:00 AM |
| Location: | Morial Convention Center - Hall F-I, Board # UU64 |
| Keywords: | multiple sclerosis, neuroprotection, vdcc, neuroinflammation |
Evidence from multiple sclerosis (MS) tissue pathology and in vivo functional studies in EAE suggests that neuronal/axonal ion channels and neurotransmitter receptors represent potential therapeutic targets in MS [Nat. Med. (2000) 6:62-66; Arch Neurol. (2002) 59:1377-80]. Voltage-dependent calcium channels (VDCCs), which mediate Ca2+ entry into cells, are implicated in gray and white matter damage in the CNS. In both MS and EAE, VDCCs are incorporated into the axoplasmic membrane, this ectopic distribution perhaps contributing to the axonal degeneration seen in these disease states [Brain (2001) 124:1114-24]. Here, we describe the effect two N-type calcium channel antagonists on the course of EAE, an animal model of MS [see also Tokuhara et al SFN 2003]. E2050 [profiled in Soc. Neurosci. Abstr. Vol 27 Prog No 332.15, 2001] and an additional compound, ER-129002-02, administered just prior to disease onset (30 and 100 mg/kg; p.o.), dose dependently reduced disease severity. Improved neurological outcome could be achieved without affecting CNS inflammation or peripheral MBP antibody production. These results substantiate the involvement of N-type Ca2+ channels in the pathogenesis of EAE and suggest that therapeutic strategies for MS should be complemented by neuroprotective measures.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
Copyright © 2003-2026 Society for Neuroscience; all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.
