Lidocaine suppresses subthreshold oscillations by inhibiting persistent Na(+) current in injured dorsal root ganglion neurons
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
17705679
DOI
10.33549/physiolres.931164
PII: 1164
Knihovny.cz E-resources
- MeSH
- Anesthetics, Local pharmacology MeSH
- Sodium Channel Blockers * MeSH
- Electrophysiology MeSH
- Data Interpretation, Statistical MeSH
- Rats MeSH
- Lidocaine pharmacology MeSH
- Membrane Potentials drug effects MeSH
- Patch-Clamp Techniques MeSH
- Neurons drug effects metabolism MeSH
- Rats, Sprague-Dawley MeSH
- Sodium Channels drug effects metabolism MeSH
- Ganglia, Spinal cytology drug effects metabolism MeSH
- In Vitro Techniques MeSH
- Tetrodotoxin pharmacology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Anesthetics, Local MeSH
- Sodium Channel Blockers * MeSH
- Lidocaine MeSH
- Sodium Channels MeSH
- Tetrodotoxin MeSH
The aim of this study was to determine the effect and mechanism of low concentration of lidocaine on subthreshold membrane potential oscillations (SMPO) and burst discharges in chronically compressed dorsal root ganglion (DRG) neurons. DRG neurons were isolated by enzymatic dissociation method. SMPO, burst discharges and single spike were elicited by whole cell patch-clamp technique in current clamp mode. Persistent Na(+) current (I(NaP)) and transient Na(+) current (I(NaT)) were elicited in voltage clamp mode. The results showed that SMPO was suppressed and burst discharges were eliminated by tetrodotoxin (TTX, 0.2 micromol/l) in current clamp mode, I(NaP) was blocked by 0.2 micromol/l TTX in voltage clamp mode. SMPO, burst discharges and I(NaP) were also suppressed by low concentration of lidocaine (10 micromol/l) respectively. However, single spike and I(NaT) could only be blocked by high concentration of lidocaine (5 mmol/l). From these results, it is suggested that I(NaP) mediates the generation of SMPO in injured DRG neurons. Low concentration of lidocaine (10 micromol/l) suppresses SMPO by selectively inhibiting I(NaP), but not I(NaT), in chronically compressed DRG neurons.
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