The effects of excessive heat on heat-activated membrane currents in cultured dorsal root ganglia neurons from neonatal rat
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
11839420
DOI
10.1016/s0304-3959(01)00401-8
PII: 00006396-200202000-00003
Knihovny.cz E-zdroje
- MeSH
- cholin farmakologie MeSH
- kapsaicin farmakologie MeSH
- kinetika MeSH
- krysa rodu Rattus MeSH
- kultivované buňky MeSH
- membránové potenciály účinky léků fyziologie MeSH
- metoda terčíkového zámku MeSH
- neurony aferentní cytologie fyziologie MeSH
- nociceptory účinky léků fyziologie MeSH
- nootropní látky farmakologie MeSH
- novorozená zvířata MeSH
- potkani Wistar MeSH
- spinální ganglia cytologie MeSH
- vápník farmakologie MeSH
- vysoká teplota MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- cholin MeSH
- kapsaicin MeSH
- nootropní látky MeSH
- vápník MeSH
The effects of high temperature (53-61 degrees C) on membrane currents (I(heat)) or depolarization (V(heat)) induced by noxious heat were studied in cultured dorsal root ganglia neurons from neonatal rats using the whole cell patch clamp technique. I(heat) or V(heat) produced by 3 s ramps of increasing temperature between 43 and 50 degrees C exhibited a fast slope (Q10>10) that was similar both during rising and falling temperature (n=85). Temperatures exceeding 52 degrees C resulted in slowdown in the recovery of I(heat), and the threshold for inducing I(heat) was shifted to lower temperatures in successive trials. These high temperatures (54-60 degrees C) caused a linear and incomplete recovery of I(heat) (Q10 decreased to <5; 4.5 +/- 0.4; n=17) and in successive trials the threshold of I(heat) decreased to temperatures close to that in the bath. The neurons, however, remained sensitive to capsaicin and to decreased extracellular pH. It is suggested that exposure of nociceptive neurons to excessive noxious heat results in an irreversible decrease of the energy barrier between the resting and activated state of the protein structures responsible for generation of I(heat). This may explain the sensitization of nociceptors after heat injury.
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