Long-lasting neuroplastic changes induced by transient decrease in
G protein-coupled receptor kinase 2 (GRK2) in nociceptors enhances and prolongs inflammatory
hyperalgesia. Here, we investigated the effects of
paroxetine (a
selective serotonin reuptake inhibitor and GRK2 inhibitor) on GRK2 expression in superior cervical ganglion (SCG) in a rat model of
complex regional pain syndrome type I (CRPS-I). After
ischemia-reperfusion (I/R) injury, the ipsilateral 50% paw withdrawal thresholds (PWTs) to mechanical stimuli and the expression levels of GRK2
protein and
mRNA in the ipsilateral SCGs all decreased significantly; the ipsilateral cold
allodynia scores increased significantly. No significant differences were found in the contralateral side except GRK2
mRNA reduced significantly at day 2-day 9 after I/R injury, but still higher than those in ipsilateral SCGs. After
paroxetine administration, the ipsilateral 50% PWTs at day 2, 7, 14, and 21 were significantly higher than those in control group; The GRK2
protein and
mRNA levels in ipsilateral SCGs were also significantly up-regulated after day1; The ipsilateral cold
allodynia scores were significantly reduced after day7. No significant differences were found in the contralateral 50% PWTs, cold
allodynia scores, and GRK2
protein level except GRK2
mRNA levels increased significantly at day1-day7 after
paroxetine administration. Therefore, a transient decrease of GRK2 expression in SCG neurons might be involved in the development and maintenance of
allodynia in CRPS-I and
paroxetine might alleviate this
allodynia through GRK2
protein upregulation in SCGs.