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- W203288017 abstract "This chapter focuses on various neuroprotective agents. The studies reviewed in the chapter range accordingly from investigations on anoxia-induced white matter injury of isolated optic nerves studied in vitro, to experiments using in vivo preparations of spinal cord and spinal nerves, to studies in whole organism level models such as experimental autoimmune encephalomyelitis (EAE). Some of these studies use anoxia or nitric oxide (NO) as triggers of axonal injury, with a basis in findings derived from human multiple sclerosis (MS) lesions. Pathological evidence indicates that some patterns of MS pathology bear close similarities to white matter hypoxic injury, and physiological studies raise the possibility that energy depletion is a contributor to axonal injury in MS. The chapter also reviews the effect of drugs and other interventions that can modulate or interfere with the axonal calcium influx cascade. These drugs and interventions include sodium channel blockers (tetrodotoxin, saxitoxin, tertiary anesthetics, anticonvulsant drugs, sodium channel blocking antiarrhythmic drugs); calcium channel blockers (dilitaizen, nifedipine, and synthetic conotoxin); blockade of Na + /Ca 2+ exchanger (bepridil, benzamil and dichlorobenzamil); and adenosine and γ-aminobutyric acid (GABA). Other mechanisms and agents include blockage of α-adrenergic receptors (prazocin), riluzole, sipatrigine, and non-glucocorticoid steroids (tirilazad mesylate). Small reductions in temperature, during anoxia-induced white matter injury, also can strongly and favorably influence nerve functional outcome." @default.
- W203288017 created "2016-06-24" @default.
- W203288017 creator A5002957653 @default.
- W203288017 creator A5010570709 @default.
- W203288017 date "2005-01-01" @default.
- W203288017 modified "2023-10-16" @default.
- W203288017 title "Blocking the Axonal Injury Cascade: Neuroprotection in Multiple Sclerosis and Its Models" @default.
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- W203288017 doi "https://doi.org/10.1016/b978-012738761-1/50030-4" @default.
- W203288017 hasPublicationYear "2005" @default.
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