Abstract
Complex regional pain syndrome type 1 (CRPS-I) is a debilitating pain condition that significantly affects life quality of patients. It remains a clinically challenging condition and the mechanisms of CRPS-I have not been fully elucidated. Here, we investigated the involvement of TRPV1, a non-selective cation channel important for integrating various painful stimuli, in an animal model of CRPS-I. A rat model of chronic post-ischemia pain (CPIP) was established to mimic CRPS-I. TRPV1 expression was significantly increased in hind paw tissue and small to medium-sized dorsal root ganglion (DRG) neurons of CPIP rats. CPIP rats showed increased TRPV1 current density and capsaicin responding rate in small-sized nociceptive DRG neurons. Local pharmacological blockage of TRPV1 with the specific antagonist AMG9810, at a dosage that does not produce hyperthermia or affect thermal perception or locomotor activity, effectively attenuated thermal and mechanical hypersensitivity in bilateral hind paws of CPIP rats and reduced the hyperexcitability of DRG neurons induced by CPIP. CPIP rats showed bilateral spinal astrocyte and microglia activations, which were significantly attenuated by AMG9810 treatment. These findings identified an important role of TRPV1 in mediating thermal and mechanical hypersensitivity in a CRPS-I animal model and further suggest local pharmacological blocking TRPV1 may represent an effective approach to ameliorate CRPS-I.
Highlights
Complex regional pain syndrome (CRPS) is a severe and debilitating pain condition which can be induced by surgery, fractures, limb trauma, ischemia or nerve lesion (Goh et al, 2017; Birklein et al, 2018)
We identified an important role of TRPV1 in mediating the behavioral hypersensitivity of chronic postischemia pain (CPIP) rat model
We found that TRPV1 protein expression was significantly increased in dorsal root ganglion (DRG) neurons that innervate the hind paw of CPIP rats
Summary
Complex regional pain syndrome (CRPS) is a severe and debilitating pain condition which can be induced by surgery, fractures, limb trauma, ischemia or nerve lesion (Goh et al, 2017; Birklein et al, 2018). CRPS can develop into chronic condition which severely affects the daily activity and life quality of the patients (Urits et al, 2018). CRPS can be further divided into two subtypes: type-I without identifiable nerve injury and type-II with identifiable nerve injury (Urits et al, 2018). Physiotherapy, sympathetic blockade, corticosteroids, and non-steroidal anti-inflammatory drugs are available treatment options for CRPS-I (Hord and Oaklander, 2003). All of these options showed inadequate therapeutic effects on CRPS-I, rendering it a clinically difficult to treat pain condition
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