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Published on: June 10, 2020
Mild Traumatic Brain Injury Contributes to the Development of Delayed Neuroinflammation
Arina Ponomarenko1, Anna Tyrtyshnaia1, Darya Ivashkevich1
1Laboratory of Pharmacology, A.V. Zhirmunsky National Scientific Center of Marine Biology, Far Eastern Branch, Russian Academy of Sciences, Vladivostok, Russian Federation.
Introduction:
In recent years, according to the literature, the problem of mild traumatic brain injury (mTBI) has become more and more urgent. Compared to moderate to severe craniocerebral trauma, mTBI occurs in a far greater number of people. The delayed sequelae caused by a single mTBI or multiple mTBIs are a significant public health problem.
Methods:
A weight-drop model was used for the formation of mTBI. A metal rod weighing 337 g with a blunt tip of 3 mm diameter was uplifted at 8 cm height and held by a lever. The trauma was created by lowering the lever and the rod and free-dropping onto the rat skull. In the cerebral cortex of experimental animals, we analyzed the level of microglial activity (Iba-1-positive system) and the expression of pro-inflammatory markers (IL1β, IL6, and CD86). Also, the expression level of the endocannabinoid system receptor (cannabinoid receptor type 1 [CB1]) was assessed in brain samples.
Results:
Experiments have shown that mTBI increases (1) the amount of microglia (iba-1) activated by the pro-inflammatory pathway (CD86); (2) the level of pro-inflammatory cytokines IL1β and IL6; and (3) CB1R activity.
Conclusion:
Overall, the results of this study indicate that mTBI induces a sustained neuroinflammatory response.
Insights
Mild traumatic brain injury (mTBI) in rats triggers a persistent neuroinflammatory response. This involves increased microglial activation, pro-inflammatory cytokines (IL1β, IL6), and cannabinoid receptor type 1 (CB1) activity, highlighting a significant public health concern.
Area of Science:
- Neuroscience
- Pathology
Background:
- Mild traumatic brain injury (mTBI) is a growing public health issue with potential long-term consequences.
- mTBI affects a large population, and its delayed effects are a significant concern.
Purpose of the Study:
- To investigate the neuroinflammatory response following mTBI in a rodent model.
- To analyze microglial activation, pro-inflammatory marker expression, and endocannabinoid system receptor activity post-mTBI.
Main Methods:
- A weight-drop model was employed to induce mTBI in rats.
- Microglial activity (Iba-1), pro-inflammatory markers (IL1β, IL6, CD86), and cannabinoid receptor type 1 (CB1) expression were assessed in brain tissue.
Main Results:
- mTBI significantly increased the number of activated microglia (Iba-1) via the pro-inflammatory pathway (CD86).
- Elevated levels of pro-inflammatory cytokines Interleukin-1 beta (IL1β) and Interleukin-6 (IL6) were observed.
- Cannabinoid receptor type 1 (CB1) activity was also found to be increased post-mTBI.
Conclusions:
- mTBI induces a sustained neuroinflammatory response.
- The findings suggest a link between mTBI, neuroinflammation, and the endocannabinoid system.
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