Wangseok Do1, Jiseok Baik1,2, Soeun Jeon1, Chang-Min You1, Dahyun Kang1, Young-Hoon Jung1, Jiyoon Lee3, Hae-Kyu Kim1,2. 1. Department of Anesthesia and Pain Medicine and Biomedical Research Institute Pusan National University Hospital, Busan, Republic of Korea. 2. Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Republic of Korea. 3. Department of Anesthesia and Pain Medicine, Seoul National University Bundang Hospital, Seongnam-si, Gyeonggi-do, Republic of Korea.
Abstract
BACKGROUND: The present study aimed to develop a rat model for mechanical allodynia after traumatic brain injury (TBI) and to investigate the expression of brain-derived neurotrophic factor (BDNF) in the cerebrospinal fluid (CSF) using this model. METHODS: A total of 180 rats were randomly allocated into three groups: a control group (group C), a sham-operated group (group S), and a controlled cortical impact induced TBI group (group T), 60 in each group. Von Frey test was performed to evaluate mechanical withdrawal thresholds. An enzyme-linked immunosorbent assay was performed to quantify BDNF level in CSF. RESULTS: The 50% withdrawal thresholds of group T were lower than those of group C and group S at all measuring points except for the preoperative period (P = 0.026, <0.001, and <0.001 for POD1, POD7, and POD14, respectively). The BDNF level of group T was higher than those of group C and group S at POD1 (P = 0.005). CONCLUSION: Upregulation of the BDNF expression in CSF was observed in rats who developed mechanical allodynia on the day after TBI. Based on our findings, to elucidate the relationship between TBI-induced neuropathic pain and BDNF expression in CSF, further research should be carried out through a multifaceted approach to a broad spectrum of pain behavior models.
BACKGROUND: The present study aimed to develop a rat model for mechanical allodynia after traumatic brain injury (TBI) and to investigate the expression of brain-derived neurotrophic factor (BDNF) in the cerebrospinal fluid (CSF) using this model. METHODS: A total of 180 rats were randomly allocated into three groups: a control group (group C), a sham-operated group (group S), and a controlled cortical impact induced TBI group (group T), 60 in each group. Von Frey test was performed to evaluate mechanical withdrawal thresholds. An enzyme-linked immunosorbent assay was performed to quantify BDNF level in CSF. RESULTS: The 50% withdrawal thresholds of group T were lower than those of group C and group S at all measuring points except for the preoperative period (P = 0.026, <0.001, and <0.001 for POD1, POD7, and POD14, respectively). The BDNF level of group T was higher than those of group C and group S at POD1 (P = 0.005). CONCLUSION: Upregulation of the BDNF expression in CSF was observed in rats who developed mechanical allodynia on the day after TBI. Based on our findings, to elucidate the relationship between TBI-induced neuropathic pain and BDNF expression in CSF, further research should be carried out through a multifaceted approach to a broad spectrum of pain behavior models.
Authors: Jeffrey T Cole; Angela Yarnell; William S Kean; Eric Gold; Bobbi Lewis; Ming Ren; David C McMullen; David M Jacobowitz; Harvey B Pollard; J Timothy O'Neill; Neil E Grunberg; Clifton L Dalgard; Joseph A Frank; William D Watson Journal: J Neurotrauma Date: 2011-03 Impact factor: 5.269