Intrathecal dexmedetomidine attenuates mechanical allodynia through the downregulation of brain-derived neurotrophic factor in a mild traumatic brain injury rat model
This study evaluated the effects of dexmedetomidine and propofol on brain-derived neurotrophic factor level in the cerebrospinal fluid (c-BDNF) and mechanical allodynia in a mild traumatic brain injury (TBI) rat model. After fixing the rat's skull on a stereotactic frame under general anesthesi...
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Published in | Korean journal of anesthesiology Vol. 76; no. 1; pp. 56 - 66 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Korea (South)
Korean Society of Anesthesiologists
01.02.2023
대한마취통증의학회 |
Subjects | |
Online Access | Get full text |
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Summary: | This study evaluated the effects of dexmedetomidine and propofol on brain-derived neurotrophic factor level in the cerebrospinal fluid (c-BDNF) and mechanical allodynia in a mild traumatic brain injury (TBI) rat model.
After fixing the rat's skull on a stereotactic frame under general anesthesia, craniotomy was performed. After impact, 10 µl of drug was injected into the cisterna magna (group S: sham, group D: dexmedetomidine 5 μg/kg, group P: propofol 500 μg/kg, and group T: untreated TBI). The 50% mechanical withdrawal threshold (50% MWT) and c-BDNF level were measured on postoperative days (PODs) 1, 7, and 14.
The 50% MWT measured on PODs 1, 7, and 14 was lower and the c-BDNF level on POD 1 was higher in group T than in group S. In group D, the c-BDNF level on POD 1 was lower than that in group T and was comparable with that in group S during the whole study period. The 50% MWT of group D was higher than that of group T throughout the postoperative period. In group P, there were no significant differences in the 50% MWT during the entire postoperative period compared with group T; the c-BDNF level was higher than that in group T on POD 1.
Intrathecal administration of dexmedetomidine may attenuate TBI-induced mechanical allodynia for up to two weeks post-injury through immediate suppression of c-BDNF in mild TBI rats. The inhibition of c-BDNF expression in the acute phase reduced the occurrence of TBI-induced chronic neuropathic pain. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 https://doi.org/10.4097/kja.22209 |
ISSN: | 2005-6419 2005-7563 2005-7563 |
DOI: | 10.4097/kja.22209 |