A single ultra-low dose or repeated administration of morphine induced hyperalgesia in mice and caused a significant increase in the levels of p-ERK and p-JNK, but not p-p38, in the spinal dorsal horn.
Our results showed that nicotine significantly reduced hyperalgesia in mice that received acute or repeated rapamycin injections, and reversed the effects of rapamycin on the phosphorylation of S6K, 4E-BP1, insulin receptor substrate-1 (IRS-1) at Ser636/639, AKT at Ser473, and ERK at Thr202/Tyr204.
The expression of p-ERK was also depressed after intrathecal injection of AMG487 associated with a significant laxation of hyperalgesia, which demonstrated that the interaction of CXCL10/CXCR3 possibly took part in neuropathic pain by regulating p-ERK signaling in the SC.
Down-regulation of HTR1As could induce VH in control rats with the increased expression of c-fos, p-ERK, and p-Akt in ACC, while up-regulation of HTR1As in the ACC could partly inhibit ACC sensitization and stress-induced visceral hyperalgesia.
Epidural treatment with osthole could ameliorate NP-evoked hyperalgesia by suppressing the activation of ERK rather than decreasing the expression of ERK protein.
This study was to investigate the role of p38 activation via ERK1/2 phosphorylation in neurons and microglia of the spinal trigeminal subnucleus caudalis (Vc) in the promotion of orofacial hyperalgesia induced by unilateral anterior crossbite (UAC) traumatic occlusion in adult rats.