Priya Chaudhary

Summary

Affiliation: Oregon Health and Science University
Country: USA

Publications

  1. ncbi request reprint 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 encephalomyelitis
    Priya 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
  2. ncbi request reprint Background potassium channel block and TRPV1 activation contribute to proton depolarization of sensory neurons from humans with neuropathic pain
    Thomas K Baumann
    Martenson Department of Neurological Surgery, Oregon Health and Science University, Portland, OR 97239 3098, USA
    Eur J Neurosci 19:1343-51. 2004
  3. pmc Cyclophilin D inactivation protects axons in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis
    Michael Forte
    Vollum Institute, Oregon Health and Science University, Portland, OR 97239, USA
    Proc Natl Acad Sci U S A 104:7558-63. 2007
  4. ncbi request reprint Expression of VPAC2 receptor and PAC1 receptor splice variants in the trigeminal ganglion of the adult rat
    Priya Chaudhary
    Department of Neurological Surgery, Oregon Health and Science University, Portland, OR 97239 3098, USA
    Brain Res Mol Brain Res 104:137-42. 2002

Detail Information

Publications4

  1. ncbi request reprint 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 encephalomyelitis
    Priya 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...
  2. ncbi request reprint Background potassium channel block and TRPV1 activation contribute to proton depolarization of sensory neurons from humans with neuropathic pain
    Thomas 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...
  3. pmc Cyclophilin D inactivation protects axons in experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis
    Michael 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...
  4. ncbi request reprint Expression of VPAC2 receptor and PAC1 receptor splice variants in the trigeminal ganglion of the adult rat
    Priya 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...