Linked Life Data

10758144

Source:http://linkedlifedata.com/resource/pubmed/id/10758144

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2000-5-15
pubmed:abstractText
In this study, we examined whether nitric oxide synthase (NOS) is upregulated in small dorsal root ganglion (DRG) neurons after axotomy and, if so, whether the upregulation of NOS modulates Na(+) currents in these cells. We identified axotomized C-type DRG neurons using a fluorescent label, hydroxystilbamine methanesulfonate and found that sciatic nerve transection upregulates NOS activity in 60% of these neurons. Fast-inactivating tetrodotoxin-sensitive (TTX-S) Na(+) ("fast") current and slowly inactivating tetrodotoxin-resistant (TTX-R) Na(+) ("slow") current were present in control noninjured neurons with current densities of 1.08 +/- 0. 09 nA/pF and 1.03 +/- 0.10 nA/pF, respectively (means +/- SE). In some control neurons, a persistent TTX-R Na(+) current was observed with current amplitude as much as approximately 50% of the TTX-S Na(+) current amplitude and 100% of the TTX-R Na(+) current amplitude. Seven to 10 days after axotomy, current density of the fast and slow Na(+) currents was reduced to 0.58 +/- 0.05 nA/pF (P < 0.01) and 0.2 +/- 0.05 nA/pF (P < 0.001), respectively. Persistent TTX-R Na(+) current was not observed in axotomized neurons. Nitric oxide (NO) produced by the upregulation of NOS can block Na(+) currents. To examine the role of NOS upregulation on the reduction of the three types of Na(+) currents in axotomized neurons, axotomized DRG neurons were incubated with 1 mM N(G)-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor. The current density of fast and slow Na(+) channels in these neurons increased to 0.82 +/- 0.08 nA/pF (P < 0.01) and 0.34 +/- 0.04 nA/pF (P < 0.05), respectively. However, we did not observe any persistent TTX-R current in axotomized neurons incubated with L-NAME. These results demonstrate that endogenous NO/NO-related species block both fast and slow Na(+) current in DRG neurons and suggest that NO functions as an autocrine regulator of Na(+) currents in injured DRG neurons.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-3077
pubmed:author
pubmed:issnType
Print
pubmed:volume
83
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2431-42
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10758144-Animals, pubmed-meshheading:10758144-Antibody Specificity, pubmed-meshheading:10758144-Autocrine Communication, pubmed-meshheading:10758144-Axotomy, pubmed-meshheading:10758144-Electrophysiology, pubmed-meshheading:10758144-Enzyme Inhibitors, pubmed-meshheading:10758144-Female, pubmed-meshheading:10758144-Ganglia, Spinal, pubmed-meshheading:10758144-Ion Channel Gating, pubmed-meshheading:10758144-Membrane Potentials, pubmed-meshheading:10758144-NG-Nitroarginine Methyl Ester, pubmed-meshheading:10758144-Neurons, Afferent, pubmed-meshheading:10758144-Nitric Oxide, pubmed-meshheading:10758144-Nitric Oxide Synthase, pubmed-meshheading:10758144-Nitric Oxide Synthase Type I, pubmed-meshheading:10758144-Rats, pubmed-meshheading:10758144-Rats, Sprague-Dawley, pubmed-meshheading:10758144-Sciatic Nerve, pubmed-meshheading:10758144-Sodium, pubmed-meshheading:10758144-Sodium Channels, pubmed-meshheading:10758144-Tetrodotoxin
pubmed:year
2000
pubmed:articleTitle
Nitric oxide is an autocrine regulator of Na(+) currents in axotomized C-type DRG neurons.
pubmed:affiliation
Department of Neurology, Yale Medical School, New Haven 06510, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't