European journal of pain : EJP
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Activation of noradrenergic α2 receptor in spinal dorsal horn effectively alleviates the pathological pain. However, the precise mechanisms underlying noradrenergic pain suppression are not fully understood. Convincing evidence has indicated that extracellular signal-regulated kinases 1 and 2 (ERK1/2) play a key role in spinal sensitization. The present study investigated the potential influence of noradrenergic α2 receptor agonist clonidine on ERK1/2 activity. ⋯ The analgesic action produced by noradrenergic α2 receptor agonist clonidine involved the reversal of ERK1/2 hyperactivity in spinal dorsal horn of inflamed mice.
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Up-regulation of voltage-gated calcium channel α2 δ1 subunit post spinal nerve ligation (SNL) injury or in α2 δ1 -overexpressing transgenic (Tg) mice correlates with tactile allodynia, a pain state mediated mainly by Aβ sensory fibres forming synaptic connections with deep dorsal horn (DDH) neurons. It is not clear, however, whether dysregulated α2 δ1 alters DDH synaptic neurotransmission that underlies tactile allodynia development post nerve injury. ⋯ Our data suggest that α2 δ1 dysregulation is highly likely contributing to tactile allodynia through a pre-synaptic mechanism involving facilitation of excitatory synaptic neurotransmission in DDH of spinal cord.
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Anticipatory postural adjustments (APAs) are motor responses generated to stabilize balance prior to voluntary movement. This study investigated how infrapatellar fat pad pain induces reorganization of APAs during reaction time tasks. It has been hypothesized that knee pain may cause insufficient APAs, thereby impairing the balance. ⋯ This study demonstrates that knee pain reorganizes the APAs which may destabilize the balance control. The knee pain-related reorganization of postural muscle activity during APA may be a part of the central modulation to maintain posture and protect the painful limb while preserving the reaction task movement performance.
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It is important to know the mechanisms underlying pain abnormalities associated with inferior alveolar nerve (IAN) regeneration in order to develop the appropriate treatment for orofacial neuropathic pain patients. However, peripheral mechanisms underlying orofacial pain abnormalities following IAN regeneration are not fully understood. ⋯ These findings suggest that the demyelination of MN fibres following regeneration may be involved in peripheral sensitization, resulting in the orofacial neuropathic pain associated with trigeminal nerve injury.