Oral administration of lithium chloride ameliorate spinal cord injury-induced hyperalgesia in male rats

Abstract

BackgroundNumerous studies have described the neuroprotective effect of lithium in spinal cord injury in addition to its ameliorative impact on pain sensation. In the present study, we aim to examine the efficacy of 85 mg/kg as well as 50 mg/kg dosage of the lithium chloride (LiCl) through oral consumption in spinal cord injured rats and their effect on gene expression of three candidate genes, corresponding to the hyper-sensitization. MethodsAdult Wistar (male) rats were divided into four experimental groups: control; oral administration of LiCl with 85 mg/kg and 50 mg/kg dosage; and 10 % sucrose receiver as the vehicle. BBB and heat plantar tests were performed weekly throughout four weeks to evaluate motor improvement and neuropathic pain amelioration, i.e., the alleviation in hyperalgesia. Then, the expression pattern of Kcnd2, ERK and Gria2 genes were assessed. ResultsThe BBB results demonstrated that LiCl with both dosages does not allow remarkable improvement in motor function during four weeks of treatment. The heat plantar tests show substantial recovery in LiCl treated groups versus vehicle and control after four weeks of evaluation. According to Real-time PCR, Kcnd2 and Gria2 were up-regulated in the presence of lithium in a dose-dependent manner while ERK expression was not differed remarkably. ConclusionOur results suggested that LiCl allows hyperalgesia palliation, however, did not reinforce persistent motor improvement. Also, oral lithium consumption with 50 mg/kg concentration, entails considerable restoration in gene expression level of Kcnd2 and Gria2.