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Anion exchanger three in dorsal root ganglion contributes to nerve injury-induced continual mechanical allodynia and thermal hyperalgesia.

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Anion exchanger three in dorsal root ganglion contributes to nerve injury-induced continual mechanical allodynia and thermal hyperalgesia.

J Pharm Pharmacol. 2018 Mar;70(three):374-382

Authors: Pérez-Rodríguez MJ, Velazquez-Lagunas I, Pluma-Pluma A, Barragán-Iglesias P, Granados-Soto V

Summary
OBJECTIVE: To find out the function of anion exchanger three (AE3) in dorsal root ganglion (DRG) in nerve injury-induced continual nociception within the rat.
METHODS: Spared nerve harm (SNI) was used to induce neuropathic ache. Von Frey filaments and Hargreaves take a look at had been used to evaluate tactile allodynia and thermal hyperalgesia, respectively. Medicine got by intrathecal administration. Western blotting was used to find out AE3 expression in DRG.
KEY FINDINGS: SNI produced long-lasting mechanical allodynia and thermal hyperalgesia. AE3 was present in DRG of sham-operated rats. SNI enhanced baseline AE3 expression in L4 and L5 DRGs at days 7 and 14, respectively. In distinction, SNI didn’t have an effect on AE3 expression in L6 DRG. AE3 expression returned to baseline ranges 21 days after SNI. Intrathecal four,four’-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS) (5-50 ?g) pretreatment prevented SNI-induced allodynia and, at a lesser extent, hyperalgesia. Furthermore, DIDS (50 ?g) diminished SNI-induced AE3 upregulation in L4, however not L5, DRGs. Intrathecal DIDS (5-50 ?g) or anti-AE3 antibody (1 ?g), however not car, post-treatment (6 days) partially reversed SNI-induced allodynia and hyperalgesia. DIDS or anti-AE3 antibody post-treatment diminished SNI-induced AE3 upregulation in L4 and L5 DRGs.
CONCLUSIONS: Information counsel that AE3 is current in DRG and contributes to mechanical allodynia and thermal hyperalgesia in neuropathic rats.

PMID: 29355942 [PubMed – indexed for MEDLINE]

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