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Verfasst von:Hoheisel, Ulrich [VerfasserIn]   i
 Mense, Siegfried [VerfasserIn]   i
Titel:Inflammation of the thoracolumbar fascia excites and sensitizes rat dorsal horn neurons
Verf.angabe:U. Hoheisel, S. Mense
E-Jahr:2015
Jahr:18 March 2015
Umfang:10 S.
Fussnoten:Gesehen am 30.11.2018
Titel Quelle:Enthalten in: European journal of pain
Ort Quelle:Malden, Mass. [u.a.] : Wiley-Blackwell, 1997
Jahr Quelle:2015
Band/Heft Quelle:19(2015), 3, Seite 419-428
ISSN Quelle:1532-2149
Abstract:Background: Recent data show that the thoracolumbar fascia can be a source of pain. However, the spinal neuronal mechanisms underlying pain from a pathologically altered fascia are unknown. The present study aimed at finding out how dorsal horn neurons react to input from a chronically inflamed thoracolumbar fascia. Methods: Recordings from rat dorsal horn neurons were made in the spinal segment L3. Twelve days before the recordings, the thoracolumbar fascia was inflamed by injection of complete Freund's adjuvant. Control animals received an injection of isotonic saline. In addition, behavioural experiments were carried out. Results: Neurons in the spinal segment L3 do not normally receive input from the fascia, but 11.1% of the neurons did when the fascia was inflamed. Compared with control, the proportion of neurons having input from all deep somatic tissues rose from 10.8% to 33.3% (p < 0.02). Moreover, many neurons acquired new deep receptive fields, most of which were located in the hindlimb (p < 0.04). Surprisingly, the pressure pain threshold of the inflamed rats did not change, but they showed a reduction in exploratory activity. Conclusions: One of the prominent findings was the appearance of new receptive fields in deep tissues of the hindlimb. Together with the expansion of the spinal target region of fascia afferents into the segment L3, the appearance of new receptive fields is a possible explanation for the spread of pain in patients with non-specific low back pain.
DOI:doi:10.1002/ejp.563
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: http://dx.doi.org/10.1002/ejp.563
 Volltext: https://onlinelibrary-wiley-com.ezproxy.medma.uni-heidelberg.de/doi/abs/10.1002/ejp.563
 DOI: https://doi.org/10.1002/ejp.563
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1584680792
Verknüpfungen:→ Zeitschrift

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