OBJECTIVES: It is now suspected that different kinds of neuropathic pain syndromes may have significantly different mechanisms. To date, much effort has been made to investigate the function of glutamate transporters (GTs) after nerve injury. The aim of this study is to compare the changes in GTs' mRNA expression levels between two distinct models of peripheral neuropathic pain: chronic constriction nerve injury (CCI) and spared nerve injury (SNI). METHODS: Experiments were performed on animal models of mononeuropathy. Several groups of rats were subjected to behavioral experiments before and 4, 7, and 14 days after the induction of mononeuropathy following the CCI and SNI. Allodynia was assessed by Von Frey filaments, and thermal hyperalgesia was assessed by the paw withdrawal tests. To study molecular experiments, the mRNA expression of (GTs) in CCI and SNI rats, reverse transcription polymerase chain reaction (RT-PCR) were used on days 4 and 14. RESULTS AND CONCLUSION: The maximum responses of mechanical allodynia and heat hyperalgesia in two distinct neuropathic pain models were detected on day 14. CCI and SNI induced upregulation of three GTs on day 4, which were followed by GTs downregulation in CCI and downregulation of glutamate aspartate transporter (GLAST) and glutamate transporter (GLT)1 in SNI when examined on day 14. These results indicate that there is an inverse correlation between pain responses and expression of GTs, and also changes in expression of spinal GTs may have a critical function in both the induction and maintenance of neuropathic pain in independent peripheral neuropathic pain models.
OBJECTIVES: It is now suspected that different kinds of neuropathic pain syndromes may have significantly different mechanisms. To date, much effort has been made to investigate the function of glutamate transporters (GTs) after nerve injury. The aim of this study is to compare the changes in GTs' mRNA expression levels between two distinct models of peripheral neuropathic pain: chronic constriction nerve injury (CCI) and spared nerve injury (SNI). METHODS: Experiments were performed on animal models of mononeuropathy. Several groups of rats were subjected to behavioral experiments before and 4, 7, and 14 days after the induction of mononeuropathy following the CCI and SNI. Allodynia was assessed by Von Frey filaments, and thermal hyperalgesia was assessed by the paw withdrawal tests. To study molecular experiments, the mRNA expression of (GTs) in CCI and SNI rats, reverse transcription polymerase chain reaction (RT-PCR) were used on days 4 and 14. RESULTS AND CONCLUSION: The maximum responses of mechanical allodynia and heat hyperalgesia in two distinct neuropathic pain models were detected on day 14. CCI and SNI induced upregulation of three GTs on day 4, which were followed by GTs downregulation in CCI and downregulation of glutamate aspartate transporter (GLAST) and glutamate transporter (GLT)1 in SNI when examined on day 14. These results indicate that there is an inverse correlation between pain responses and expression of GTs, and also changes in expression of spinal GTs may have a critical function in both the induction and maintenance of neuropathic pain in independent peripheral neuropathic pain models.