Abstract：
:Protection of CNS white matter tracts in brain and spinal cord is essential for maximizing clinical recovery from disorders such as stroke or spinal cord injury. Central myelinated axons are damaged by anoxia/ischemia in a Ca(2+)-dependent manner. Leakage of Na+ into the axoplasm through Na+ channels causes Ca2+ overload mainly by reverse Na(+)-Ca2+ exchange. Na+ channel blockers have thus been shown to be protective in an in vitro anoxic rat optic nerve model. Mexiletine (10 microM-1 mM), an antiarrhythmic and use-dependent Na+ channel blocker, was also significantly protective, as measured by recovery of the compound action potential after a 60 min anoxic exposure in vitro. More importantly, mexiletine (80 mg/kg, i.p.) also significantly protected optic nerves from injury in a model of in situ ischemia. This in situ model is more clinically relevant as it addresses drug pharmacokinetics, toxicity and CNS penetration. Optic nerve recovery cycles (defined as shifts in latency of compound action potentials with paired stimulation) were used to measure the concentration of mexiletine in optic nerves after systemic administration, estimated at approximately 42 microM 1 h after a single dose of 80 mg/kg, i.p. These results indicate that mexiletine is able to penetrate into the CNS at concentrations sufficient to confer significant protection. Na+ channel blockers such as mexiletine may prove to be effective clinical therapeutic agents for protecting CNS white matter tracts against anoxic/ischemic injury.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Stys PK,Lesiuk Hdoi
10.1016/0306-4522(95)00430-0subject
Has Abstractpub_date
1996-03-01 00:00:00pages
27-36issue
1eissn
0306-4522issn
1873-7544pii
0306-4522(95)00430-0journal_volume
71pub_type
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