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Modulation of blood-brain barrier dysfunction and neurological deficits during acute experimental allergic encephalomyelitis by the N-methyl-D-aspartate receptor antagonist memantine.
Therapeutic application of memantine was found to be as effective as semiprophylactic dosing, suggesting the NMDA receptor as a viable pharmacological target for future treatment of human neurological conditions such as multiple sclerosis. Expand
Glutamate Receptors in Neuroinflammatory Demyelinating Disease
The importance of the glutamate receptors in EAE and MS pathogenesis is considered, and the use of receptor antagonists to control EAE is also discussed together with the possibility of therapeutic application in demyelinating disease. Expand
Inhibition of blood-brain barrier disruption in experimental allergic encephalomyelitis by short-term therapy with dexamethasone or cyclosporin A.
Therapeutically administered dexamethasone or cyclosporin A dose-dependently reduced albumin movement across the blood-brain barrier (BBB) and suppressed abnormal BBB permeability in all tissues. Expand
MK-801 limits neurovascular dysfunction during experimental allergic encephalomyelitis.
The use of MK-801 to control major features of EAE strongly implicates N-methyl-D-aspartate receptor-dependent mechanisms in disease development and prompts consideration of a role for the receptor in the pathogenesis of human demyelinating conditions. Expand
The detection and quantitation of inflammation in the central nervous system during experimental allergic encephalomyelitis using the radiopharmaceutical 99mTc-RP128
- C. Paul, S. Peers, Lesley E. Woodhouse, J. Thornback, A. Goodbody, C. Bolton
- Journal of Neuroscience Methods
- 15 May 2000
The rapid in vivo labelling by 99mTc-RP128 of specific inflammatory cells combined with the ability to monitor the progress of anti-inflammatory therapeutics may recommend the agent for use in a variety of inflammatory conditions. Expand
Aspects of the biochemical pharmacology of neurovascular disruption in experimental allergic encephalomyelitis (EAE)
The endothelium and inflammation
Protective endothelial adaptation to chronic inflammation exists, with related mechanisms inhibiting persistent complement-mediated endothelial activation, and retention of activated neutrophils undergoing this dis-regulated apoptosis may contribute to endothelial cell damage in inflammation in the kidney. Expand
Antagonism of N-methyl-D-aspartate (NMDA) receptor activity with memantine limits blood-brain barrier (BBB) dysfunction and disease development during experimental allergic encephalomyelitis (EAE)
This study highlights the importance of knowing the carrier and removal status of canine coronavirus, as a source of infection for other animals, not necessarily belonging to the same breeds. Expand
N-methyl-D-aspartate receptor-mediated events contribute to neurovascular breakdown during experimental allergic encephalomyelitis.
Adrenomedullin receptors on human T cells are glucocorticoid-sensitive.
The findings indicate that human T cells utilize both AM(1) and AM(2) receptors, which are GC-sensitive in an activation-state dependent manner. Expand