Neuroreport 2003 Mar 24;14(4):555-8
Craner MJ, Lo AC, Black JA, Baker D, Newcombe J, Cuzner ML, Waxman SG.
1Department of Neurology and PVA/EPVA Center for Neuroscience Research, Yale University School of Medicine, 333 Cedar Street, P.O. Box 208018, New Haven, CT 06520-8018 2Rehabilitation Research Center, VA Hospital, West Haven, CT 06516, USA.
The sensory neuron specific sodium channel Na(v)1.8 is normally detectable at only very low levels within cerebellar Purkinje cells.
Annexin II light chain (p11) binds to the amino terminus of Na(v)1.8 and facilitates its functional expression within the cell membrane.
We previously demonstrated that expression of Na(v)1.8 is up-regulated in cerebellar Purkinje cells in experimental allergic encephalomyelitis (EAE) and multiple sclerosis (MS).
In this study we demonstrate that expression of p11 is significantly up-regulated in Purkinje cells in EAE (71 +/- 9.0% vs 21.3 +/- 4.9% in controls) and in MS(65.5 +/- 1.6% vs 21.8 +/- 6.2% in controls).
We also demonstrate a high degree of co-expression of p11 and Na(v)1.8 (84.8 +/- 8.9%).
Together with earlier results which show that experimental expression of Na(v)1.8 within Purkinje cells perturbs the temporal pattern of impulse generation in these cells, our results extend the evidence for an acquired channelopathy which interferes with cerebellar function in MS.