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. 2022 Jan 29:15:229-239.
doi: 10.2147/JPR.S344110. eCollection 2022.

Increased Brain-Derived Neurotrophic Factor Levels in Cerebrospinal Fluid During the Acute Phase in TBI-Induced Mechanical Allodynia in the Rat Model

Wangseok Do  1 , Jiseok Baik  1   2 , Soeun Jeon  1 , Chang-Min You  1 , Dahyun Kang  1 , Young-Hoon Jung  1 , Jiyoon Lee  3 , Hae-Kyu Kim  1   2
Affiliations

Increased Brain-Derived Neurotrophic Factor Levels in Cerebrospinal Fluid During the Acute Phase in TBI-Induced Mechanical Allodynia in the Rat Model

Wangseok Do et al. J Pain Res. .

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.

Keywords: animal; brain injuries; brain-derived neurotrophic factor; models; nerve growth factors; neuralgia; traumatic.

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Conflict of interest statement

Prof. Dr. Wangseok Do reports grants from National Research Foundation of Korea (NRF) grant funded by the Korean government (Ministry of Science and ICT), during the conduct of the study. Dr Soeun Jeon reports grants from National Research Foundation of Korea (NRF) grant funded by the Korean government (Ministry of Science and ICT), during the conduct of the study. Dr Chang-Min You reports grants from National Research Foundation of Korea (NRF) grant funded by the Korean government (Ministry of Science and ICT), during the conduct of the study. Dr Dahyun Kang reports grants from National Research Foundation of Korea (NRF) grant funded by the Korean government (Ministry of Science and ICT), during the conduct of the study. Dr Jiyoon Lee reports grants from Pusan National University Hospital, grants from Korean government, during the conduct of the study. The authors report no conflicts of interest in this work.

Figures

Figure 1
Figure 1
Delivery of controlled cortical impact in a rat model of traumatic brain injury. We used the controlled cortical impact method to develop a rat model of neuropathic pain after traumatic brain injury. (A–C) After anesthesia with isoflurane, the rat’s head was securely fixed to the stereotactic frame in a prone position. A craniotomy was performed, and the impact was delivered (depth 2.5 mm, velocity 3 m/s, and dwell time 85 ms). (D) The controlled cortical impact device with a stereotactic frame (Pinpoint PCI3000 Precision Cortical Impactor; Hatteras Instruments, Cary, NC, USA).
Figure 2
Figure 2
Cerebrospinal fluid sampling in this rat model. (A) An anatomical landmark approach was employed to identify the puncture site above the atlanto-occipital joint in the middle of a triangle between the occipital protuberance and the most prominent points of the transverse processes of the atlas. (B and C) A 27G needle connected to a syringe bevel-down was vertically inserted into the puncture site and advanced to the cisterna magna.
Figure 3
Figure 3
Flow of 180 Sprague-Dawley rats through this study on brain-derived neurotrophic factor levels after traumatic brain injury.
Figure 4
Figure 4
Flow chart of subgroup analysis.
See this image and copyright information in PMC

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References

    1. Xiong Y, Mahmood A, Chopp M. Animal models of traumatic brain injury. Nat Rev Neurosci. 2013;14(2):128–142. doi:10.1038/nrn3407 - DOI - PMC - PubMed
    1. Jung HY, Han SH. Depression after traumatic brain injury. Korean J Biol Psychiatry. 1999;6(1):21–29.
    1. Harrison-Felix CL, Whiteneck GG, Jha A, DeVivo MJ, Hammond FM, Hart DM. Mortality over four decades after traumatic brain injury rehabilitation: a Retrospective Cohort Study. Arch Phys Med Rehabil. 2009;90(9):1506–1513. doi:10.1016/j.apmr.2009.03.015 - DOI - PubMed
    1. Irvine KA, Clark DJ. Chronic pain after traumatic brain injury: pathophysiology and pain mechanisms. Pain Med. 2018;19(7):1315–1333. doi:10.1093/pm/pnx153 - DOI - PubMed
    1. Nampiaparampil DE. Prevalence of chronic pain after traumatic brain injury: a systematic review. JAMA. 2008;300(6):711–719. doi:10.1001/jama.300.6.711 - DOI - PubMed