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Erschienen in: Experimental Brain Research 3/2003

01.06.2003 | Research Article

Voltage-gated calcium channels may be involved in the regulation of the mechanosensitivity of slowly conducting knee joint afferents in rat

verfasst von: Stefan Just, Bernd Heppelmann

Erschienen in: Experimental Brain Research | Ausgabe 3/2003

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Abstract

Voltage-gated Ca2+ channels play an important role in the central processing of nociceptive information. Recently, it has been shown that L- and N-type voltage-gated Ca2+ channels are also present on peptidergic, fine afferent nerve fibers in the knee joint capsule. Therefore, the influence of specific blockers for L-type (verapamil) or N-type (ω-conotoxin GVIA) Ca2+ channels on the mechanosensitivity of slowly conducting afferents was tested in the rat knee joint. Topical application of 100 μM verapamil onto the receptive field reduced the mean response to knee joint rotation to 67±8% (SEM, n=12), obtained by outward rotations with a torque of 10 mNm above the mechanical threshold and compared with control movements. In the presence of 50 μM ω-conotoxin GVIA, the mean response decreased to 44±5% (n=12), a reduction that was also observed during rotations of other intensities. Simultaneous application of both substances further reduced the response to 25±11% (n=6). In additional experiments it was shown that L- and N-type voltage-gated Ca2+ channels do not influence activity-dependent changes of the mechanical excitability. In conclusion, the data of the present study indicate that voltage-gated Ca2+ channels may also be involved in the regulation of the mechanosensitivity of nociceptive nerve fiber endings.
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Metadaten
Titel
Voltage-gated calcium channels may be involved in the regulation of the mechanosensitivity of slowly conducting knee joint afferents in rat
verfasst von
Stefan Just
Bernd Heppelmann
Publikationsdatum
01.06.2003
Verlag
Springer-Verlag
Erschienen in
Experimental Brain Research / Ausgabe 3/2003
Print ISSN: 0014-4819
Elektronische ISSN: 1432-1106
DOI
https://doi.org/10.1007/s00221-003-1465-x

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