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Updated: May 22, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Developmental traumatic brain injury decreased brain derived neurotrophic factor expression late after injury
Michelle Elena Schober1, Benjamin Block, Daniela F Requena
1University of Utah, Salt Lake City, USA. michelle.schober@hsc.utah.edu
Insights
Traumatic brain injury (TBI) in young rats did not increase hippocampal Brain Derived Neurotrophic Factor (BDNF) after injury. However, TBI did decrease BDNF protein levels 14 days post-injury, indicating potential long-term effects.
Area of Science:
- Neuroscience
- Developmental Biology
- Traumatic Brain Injury Research
Background:
- Pediatric traumatic brain injury (TBI) is a leading cause of acquired cognitive impairment in children.
- Hippocampal Brain Derived Neurotrophic Factor (BDNF) plays a crucial role in cognitive function.
- The impact of TBI on BDNF levels in the developing hippocampus remains largely unexplored.
Purpose of the Study:
- To investigate the effects of controlled cortical impact (CCI) on hippocampal BDNF mRNA and protein levels in 17-day-old rat pups.
- To determine if CCI alters BDNF expression at early (post-injury day 2) and later (post-injury day 14) time points.
- To compare BDNF levels in TBI, sham-operated, and naïve control groups.
Main Methods:
- Controlled cortical impact (CCI) model in 17-day-old rat pups.
- Measurement of hippocampal BDNF mRNA and protein levels at various post-injury days (PID 1, 2, 3, 7, 14).
- Comparison of BDNF expression between CCI, SHAM (sham-operated), and Naïve (unoperated) groups.
Main Results:
- CCI did not alter hippocampal BDNF mRNA or protein levels by post-injury day 2 compared to SHAM.
- BDNF protein levels were decreased in the injured hippocampus by post-injury day 14 in CCI rats relative to SHAM.
- Both CCI and SHAM procedures led to decreased BDNF mRNA and protein levels at various time points compared to Naïve controls.
Conclusions:
- TBI in developing rats resulted in decreased hippocampal BDNF protein 14 days after injury.
- The experimental procedures themselves (craniotomy, anesthesia, maternal separation) may independently reduce BDNF expression in the developing hippocampus.
- Future studies on TBI and BDNF in developing brains should include a Naïve group and carefully consider the experimental paradigm's influence.
Abstract:
Pediatric traumatic brain injury (TBI) is a major cause of acquired cognitive dysfunction in children. Hippocampal Brain Derived Neurotrophic Factor (BDNF) is important for normal cognition. Little is known about the effects of TBI on BDNF levels in the developing hippocampus. We used controlled cortical impact (CCI) in the 17 day old rat pup to test the hypothesis that CCI would first increase rat hippocampal BDNF mRNA/protein levels relative to SHAM and Naïve rats by post injury day (PID) 2 and then decrease BDNF mRNA/protein by PID14. Relative to SHAM, CCI did not change BDNF mRNA/protein levels in the injured hippocampus in the first 2 days after injury but did decrease BDNF protein at PID14. Surprisingly, BDNF mRNA decreased at PID 1, 3, 7 and 14, and BDNF protein decreased at PID 2, in SHAM and CCI hippocampi relative to Naïve. In conclusion, TBI decreased BDNF protein in the injured rat pup hippocampus 14 days after injury. BDNF mRNA levels decreased in both CCI and SHAM hippocampi relative to Naïve, suggesting that certain aspects of the experimental paradigm (such as craniotomy, anesthesia, and/or maternal separation) may decrease the expression of BDNF in the developing hippocampus. While BDNF is important for normal cognition, no inferences can be made regarding the cognitive impact of any of these factors. Such findings, however, suggest that meticulous attention to the experimental paradigm, and possible inclusion of a Naïve group, is warranted in studies of BDNF expression in the developing brain after TBI.
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