Blocking the Axonal Injury Cascade: Neuroprotection in Multiple Sclerosis and Its Models

摘要: This chapter focuses on various neuroprotective agents. The studies reviewed in the range accordingly from investigations anoxia-induced white matter injury of isolated optic nerves studied vitro, to experiments using vivo preparations spinal cord and nerves, whole organism level models such as experimental autoimmune encephalomyelitis (EAE). Some these use anoxia or nitric oxide (NO) triggers axonal injury, with a basis findings derived human multiple sclerosis (MS) lesions. Pathological evidence indicates that some patterns MS pathology bear close similarities hypoxic physiological raise possibility energy depletion is contributor MS. also reviews effect drugs other interventions can modulate interfere calcium influx cascade. These include sodium channel blockers (tetrodotoxin, saxitoxin, tertiary anesthetics, anticonvulsant drugs, blocking antiarrhythmic drugs); (dilitaizen, nifedipine, synthetic conotoxin); blockade Na + /Ca 2+ exchanger (bepridil, benzamil dichlorobenzamil); adenosine γ-aminobutyric acid (GABA). Other mechanisms agents blockage α-adrenergic receptors (prazocin), riluzole, sipatrigine, non-glucocorticoid steroids (tirilazad mesylate). Small reductions temperature, during strongly favorably influence nerve functional outcome.