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Molecular Pain

, 7:59

First Online: 16 August 2011Received: 08 July 2011Accepted: 16 August 2011

Abstract

Cellular prion protein PrP inhibits N-Methyl-D-Aspartate NMDA receptors. Since NMDA receptors play an important role in the transmission of pain signals in the dorsal horn of spinal cord, we thus wanted to determine if PrP null mice show a reduced threshold for various pain behaviours.

We compared nociceptive thresholds between wild type and PrP null mice in models of inflammatory and neuropathic pain, in the presence and the absence of a NMDA receptor antagonist. 2-3 months old male PrP null mice exhibited an MK-801 sensitive decrease in the paw withdrawal threshold in response both mechanical and thermal stimuli. PrP null mice also exhibited significantly longer licking-biting time during both the first and second phases of formalin-induced inflammation of the paw, which was again prevented by treatment of the mice with MK-801, and responded more strongly to glutamate injection into the paw. Compared to wild type animals, PrP null mice also exhibited a significantly greater nociceptive response licking-biting after intrathecal injection of NMDA. Sciatic nerve ligation resulted in MK-801 sensitive neuropathic pain in wild-type mice, but did not further augment the basal increase in pain behaviour observed in the null mice, suggesting that mice lacking PrP may already be in a state of tonic central sensitization. Altogether, our data indicate that PrP exerts a critical role in modulating nociceptive transmission at the spinal cord level, and fit with the concept of NMDA receptor hyperfunction in the absence of PrP.

KeywordsPrion protein pain knockout mice NMDA receptor spinal cord Electronic supplementary materialThe online version of this article doi:10.1186-1744-8069-7-59 contains supplementary material, which is available to authorized users.

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Autor: Vinicius M Gadotti - Gerald W Zamponi

Fuente: https://link.springer.com/



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