Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2002 Aug;75(2):193-9.
doi: 10.1006/exer.2002.2014.

Molecular identities of two tetrodotoxin-resistant sodium channels in corneal axons

Affiliations

Molecular identities of two tetrodotoxin-resistant sodium channels in corneal axons

Joel A Black et al. Exp Eye Res. 2002 Aug.

Abstract

Previous electrophysiological studies have demonstrated that tetrodotoxin-resistant (TTX-R) sodium channels contribute to action potential electrogenesis and conduction along non-myelinated PNS axons. Moreover, recent work has established that TTX-R sodium channels play a major role in the generation of action potentials in the terminals of non-myelinated nociceptive axons innervating the cornea. We have utilized subtype-specific antibodies to sodium channels Na(v)1.8 and Na(v)1.9 to examine the molecular identity of the TTX-R sodium channels that are present in these axons. Both Na(v)1.8 and Na(v)1.9 sodium channels are expressed diffusely along the entire lengths of non-myelinated corneal axons, from the nerve plexus at the corneoscleral limbus to the distal corneal leash fibers. Moreover, both Na(v)1.8 and Na(v)1.9 are localized at the bulb-like nerve terminals of the leash fibers within the superficial epithelial layers of the cornea. These observations suggest that both TTX-R sodium channels Na(v)1.8 and Na(v)1.9 contribute to the electrogenesis of non-myelinated axons of the cornea.

PubMed Disclaimer

Publication types

LinkOut - more resources