Noninactivating, tetrodotoxin-sensitive Na+ conductance in rat optic nerve axons

摘要: The ionic current underlying the upstroke of axonal action potentials is carried by rapidly activating, voltage-dependent Na+ channels. Termination potential mediated in part rapid inactivation these We previously demonstrated that an influx plays a critical role cascade leading to irreversible anoxic injury central nervous system white matter. speculated noninactivating conductance mediates this pathological and persists at depolarized membrane as seen axons. In present study we measured resting compound rat optic nerves using modified "grease-gap" technique. Application tetrodotoxin (2 microM) ([K+]o = 3 mM) or 15 40 mM K+ resulted hyperpolarizing shifts potential. interpret evidence for persistent, conductance. This rest sufficiently abolish classical transient currents. PK/PNa ratios were estimated 35.5, 23.2, 88 mM, K+, respectively. suggest may provide inward pathway ions, necessary operation Na+, K(+)-ATPase. Under conditions, such anoxia, likely route influx, which causes damaging Ca2+ entry through reverse Na(+)-Ca2+ exchanger. presence matter axons therapeutic opportunity diseases stroke spinal cord injury.