Affiliation: Oregon Health and Science University
- Lipoic acid inhibits expression of ICAM-1 and VCAM-1 by CNS endothelial cells and T cell migration into the spinal cord in experimental autoimmune encephalomyelitisPriya Chaudhary
Department of Neurology, L226, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, 97239, USA
J Neuroimmunol 175:87-96. 2006..Overall, our data suggest that the anti-inflammatory effects of LA in EAE may be partly due to inhibition of ICAM-1 and VCAM-1 expression by central nervous system (CNS) endothelial cells...
- Background potassium channel block and TRPV1 activation contribute to proton depolarization of sensory neurons from humans with neuropathic painThomas K Baumann
Martenson Department of Neurological Surgery, Oregon Health and Science University, Portland, OR 97239 3098, USA
Eur J Neurosci 19:1343-51. 2004..We conclude that in most neurons the sustained depolarization in response to moderately acidic solutions is the result of blocked background potassium channels. In a subset of neurons, TRPV1 also contributes...
- Cyclophilin D inactivation protects axons in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosisMichael Forte
Vollum Institute, Oregon Health and Science University, Portland, OR 97239, USA
Proc Natl Acad Sci U S A 104:7558-63. 2007..Our results directly implicate pathological activation of the mitochondrial PTP in the axonal damage occurring during MS and identify CyPD, as well as the PTP, as a potential target for MS neuroprotective therapies...
- Expression of VPAC2 receptor and PAC1 receptor splice variants in the trigeminal ganglion of the adult ratPriya Chaudhary
Department of Neurological Surgery, Oregon Health and Science University, Portland, OR 97239 3098, USA
Brain Res Mol Brain Res 104:137-42. 2002..Immunocytochemistry showed PAC1 and VPAC2 to be present in small-diameter TG neurons. Thus, PACAP and VIP are potential mediators of cross-excitation in the TG...