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Updated: Oct 17, 2026
A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury
Published on: June 20, 2017
Possible roles of COX-1 in learning and memory impairment induced by traumatic brain injury in mice
Abstract:
People who suffer from traumatic brain injury (TBI) often experience cognitive deficits in spatial reference and working memory. The possible roles of cyclooxygenase-1 (COX-1) in learning and memory impairment in mice with TBI are far from well known. Adult mice subjected to TBI were treated with the COX-1 selective inhibitor SC560. Performance in the open field and on the beam walk was then used to assess motor and behavioral function 1, 3, 7, 14, and 21 days following injury. Acquisition of spatial learning and memory retention was assessed using the Morris water maze on day 15 post-TBI. The expressions of COX-1, prostaglandin E2 (PGE2), interleukin (IL)-6, brain-derived neurotrophic factor (BDNF), platelet-derived growth factor BB (PDGF-BB), synapsin-I, and synaptophysin were detected in TBI mice. Administration of SC560 improved performance of beam walk tasks as well as spatial learning and memory after TBI. SC560 also reduced expressions of inflammatory markers IL-6 and PGE2, and reversed the expressions of COX-1, BDNF, PDGF-BB, synapsin-I, and synaptophysin in TBI mice. The present findings demonstrated that COX-1 might play an important role in cognitive deficits after TBI and that selective COX-1 inhibition should be further investigated as a potential therapeutic approach for TBI.
Insights
Cyclooxygenase-1 (COX-1) inhibition improved cognitive deficits and motor function in mice with traumatic brain injury (TBI). Selective COX-1 inhibition may offer a new therapeutic strategy for TBI recovery.
Area of Science:
- Neuroscience
- Pharmacology
- Pathology
Background:
- Traumatic brain injury (TBI) frequently leads to cognitive impairments, particularly in spatial reference and working memory.
- The specific role of cyclooxygenase-1 (COX-1) in TBI-induced learning and memory deficits remains largely uncharacterized.
Purpose of the Study:
- To investigate the involvement of COX-1 in cognitive dysfunction following TBI in a mouse model.
- To evaluate the therapeutic potential of a selective COX-1 inhibitor, SC560, in mitigating TBI-related deficits.
Main Methods:
- Adult mice underwent TBI and were subsequently treated with the selective COX-1 inhibitor SC560.
- Motor and behavioral functions were assessed using open field and beam walk tests.
- Spatial learning and memory were evaluated using the Morris water maze.
- Expressions of COX-1, PGE2, IL-6, BDNF, PDGF-BB, synapsin-I, and synaptophysin were quantified.
Main Results:
- SC560 administration significantly improved performance in beam walk tasks and enhanced spatial learning and memory retention post-TBI.
- SC560 treatment reduced the expression of inflammatory markers (IL-6, PGE2) and normalized the expression of COX-1, BDNF, PDGF-BB, synapsin-I, and synaptophysin in TBI mice.
Conclusions:
- COX-1 plays a significant role in the cognitive deficits observed after TBI.
- Selective inhibition of COX-1 presents a promising therapeutic avenue for managing cognitive impairments associated with TBI.
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