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Digitale Medien

Proton-induced calcitonin gene-related peptide release from rat sciatic nerve axons, in vitro, involving TRPV1 (2003)

Fischer, Michael J. M. ; Reeh, Peter W. ; Sauer, Susanne K.

Oxford, UK : Blackwell Science Ltd

European journal of neuroscience 18 (2003), S. 0

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ISSN: 1460-9568

Quelle: Blackwell Publishing Journal Backfiles 1879-2005

Thema: Medizin

Notizen: We have shown previously that rat sciatic nerve axons in vitro express sensitivity to capsaicin and heat and responded to these stimuli with a Ca2+-dependent and graded immunoreactive calcitonin gene-related peptide release. Morphological evidence for stimulated vesicular exocytosis and for the vanilloid receptor TRPV1 in the axolemma of the unmyelinated nerve fibres has also been presented. Here we used solutions of low pH, high K+ or 47 °C to stimulate isolated desheathed sciatic nerves measuring immunoreactive calcitonin gene-related peptide release. pH 6.1 increased immunoreactive calcitonin gene-related peptide release by 31% over baseline and pH 5.2 and 4.3 caused a log-linear concentration-dependent increase of 137 and 265%, respectively. The effect of pH 3.4 was out of the linear range and not reversible. Stimulation in Ca2+-free solutions and under increased intracellular Ca2+ buffering capacity strongly reduced the proton responses. The TRPV1 antagonists capsazepine and ruthenium red substantially reduced the effects of pH 5.2 but not pH 6.1. Combining a stimulus of 60 mm K+ with the subliminal pH 6.3 reduced the axonal immunoreactive calcitonin gene-related peptide response by 88%. The noxious heat response at pH 6.3, however, was only reduced by 39%, suggesting a hidden sensitization to heat by low pH. This was supported by an effect of capsazepine to reduce the combined response to half, indicative of an involvement of TRPV1 in the sensitization but not in the axonal heat response itself that was found to be resistant to capsazepine. Axonal calcitonin gene-related peptide release is thought to play a physiological role in activity-dependent autoregulation of endoneurial blood flow. Axonal sensitivity to and sensitization by protons may be a pathophysiological mechanism involved in certain peripheral neuropathies.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1046/j.1460-9568.2003.02811.x

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Digitale Medien

Bradykinin-induced nociceptor sensitization to heat is mediated by cyclooxygenase products in isolated rat skin (2001)

Pethö, Gabor ; Derow, Alexandra ; Reeh, Peter W.

Oxford, UK : Blackwell Science Ltd

European journal of neuroscience 14 (2001), S. 0

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ISSN: 1460-9568

Quelle: Blackwell Publishing Journal Backfiles 1879-2005

Thema: Medizin

Notizen: Bradykinin can excite C-polymodal nociceptors and sensitize them to heat and it can also enhance prostaglandin synthesis, but it is unclear whether these effects are causally related. The role of cyclooxygenase products was investigated using two enantiomers of the cyclooxygenase inhibitor flurbiprofen of which S(+)- is more potent than R(–)-flurbiprofen. Single-unit activity was recorded from mechano-heat-sensitive, polymodal C-fibers in the isolated rat skin-saphenous nerve preparation. Bradykinin pretreatment (10 µm, 5 min) induced a 219 ± 26% increase in the number of spikes evoked by noxious heat stimulation and a drop in the heat threshold by 5.2 ± 0.6 °C in a fully reproducible manner. S(+)-flurbiprofen (1 µm) abolished the bradykinin-induced heat sensitization but did not alter the unconditioned heat response itself. Under R(–)-flurbiprofen (1 µm) bradykinin still induced a significant heat sensitization which was reduced by 33 ± 21% (P = 0.11) of its previous extent; this effect may be due to the limited purity of the enantiomer preparation or to a cyclooxygenase-independent action of flurbiprofen. The heat sensitization suppressed by S(+)-flurbiprofen could be significantly restored (to 43 ± 12%) by addition of PGE2 plus PGI2 (10 µm both) to bradykinin. Neither S(+)- nor R(–)-flurbiprofen had an influence on the magnitude of the excitatory effect of bradykinin. It is concluded that (i) cyclooxygenase products are the main mediators of nociceptor sensitization to heat following bradykinin treatment in the isolated rat skin; (ii) PGE2/I2 are essential but perhaps not the only relevant cyclooxygenase products involved and (iii) neither S(+)- nor R(–)-flurbiprofen inhibit the unconditioned noxious heat response and the excitatory bradykinin response of the polymodal C-nociceptors.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1046/j.0953-816x.2001.01651.x

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Digitale Medien

Sensory neuron sodium channel Na v 1.8 is essential for pain at low temperatures (2007)

Leffler, Andreas ; Babes, Alexandru ; Cendan, Cruz Miguel ; [weitere]

[s.l.] : Nature Publishing Group

Nature 447 (2007), S. 856-859

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ISSN: 1476-4687

Quelle: Nature Archives 1869 - 2009

Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik

Notizen: [Auszug] Sensory acuity and motor dexterity deteriorate when human limbs cool down, but pain perception persists and cold-induced pain can become excruciating. Evolutionary pressure to enforce protective behaviour requires that damage-sensing neurons (nociceptors) continue to function at low ...

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1038/nature05880

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