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

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

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

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Stys, P. K. Sontheimer, H. Ransom, B. R. Waxman, S. G.
Description	Author Affiliation: Stys PK ( Department of Neurology, Yale School of Medicine, New Haven, CT 06510.);
Abstract	The ionic current underlying the upstroke of axonal action potentials is carried by rapidly activating, voltage-dependent Na+ channels. Termination of the action potential is mediated in part by the rapid inactivation of these Na+ channels. We previously demonstrated that an influx of Na+ plays a critical role in the cascade leading to irreversible anoxic injury in central nervous system white matter. We speculated that a noninactivating Na+ conductance mediates this pathological Na+ influx and persists at depolarized membrane potentials as seen in anoxic axons. In the present study we measured the resting compound membrane potential of rat optic nerves using a modified 'grease-gap' technique. Application of tetrodotoxin (2 microM) to resting nerves ([K+]o = 3 mM) or to nerves depolarized by 15 or 40 mM K+ resulted in hyperpolarizing shifts of membrane potential. We interpret these shifts as evidence for a persistent, noninactivating Na+ conductance. This conductance is present at rest and persists in nerves depolarized sufficiently to abolish classical transient Na+ currents. PK/PNa ratios were estimated at 35.5, 23.2, and 88 in 3 mM, 15 mM, and 40 mM K+, respectively. We suggest that this noninactivating Na+ conductance may provide an inward pathway for Na+ ions, necessary for the operation of Na+, K(+)-ATPase. Under pathological conditions, such as anoxia, this conductance is the likely route of Na+ influx, which causes damaging Ca2+ entry through reverse operation of the Na(+)-Ca2+ exchanger. The presence of this conductance in white matter axons may provide a therapeutic opportunity for diseases such as stroke and spinal cord injury.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	15
Volume Number	90
Language	English
Publisher	National Academy of Sciences
Publisher Date	1993-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Anoxia Physiopathology Optic Nerve Physiology Sodium Channels Drug Effects Sodium Tetrodotoxin Pharmacology Animals Electric Conductivity In Vitro Techniques Membrane Potentials Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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