Abstract

An early step in repair of the leech CNS is the appearance of endothelial nitric oxide synthase (eNOS) immunoreactivity and NOS activity, but coincident generation of NO at the lesion after injury has not been shown. This is important because NO can regulate microglial cell motility and axon growth. Indirect measurement of NO with the standard citrulline assay demonstrated that NO was generated within 30 min after nerve cord injury. A polarographic NO-selective self-referencing microelectrode that measures NO flux noninvasively was developed to obtain higher spatial and temporal resolution. With this probe, it was possible to demonstrate that immediately after the leech CNS was injured, NO left the lesion with a mean peak efflux of 803 ± 99 fmol NO cm-2 sec-1. NO efflux exponentially declined to a constant value, as described through the equation f(t) = y0 + ae-t/τ, with τ = 117 ± 30 sec. The constant Y0 = 15.8 ± 4.5 fmol cm-2 represents a sustained efflux of NO. Approximately 200 pmol NO cm-2 is produced at the lesion (n = 8). Thus, injury activates eNOS already present in the CNS and precedes the accumulation of microglia at the lesion, consistent with the hypothesis that NO acts to stop the migrating microglia at the lesion site.

Department(s)

Biological Sciences

Comments

National Institute of Neurological Disorders and Stroke, Grant R01NS034927

Keywords and Phrases

Endothelial nitric oxide synthase (eNOS); Leech CNS; Microglia; Nerve injury; Nerve repair; Nitric oxide (NO); NO efflux; NO-selective microsensor; Regeneration

International Standard Serial Number (ISSN)

0270-6474

Document Type

Article - Journal

Document Version

Final Version

File Type

text

Language(s)

English

Rights

© 2024 The Authors, All rights reserved.

Creative Commons Licensing

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.

Publication Date

01 Jan 2001

PubMed ID

11150338

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