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Updated: Feb 17, 2026
Electromagnetic Controlled Closed-Head Model of Mild Traumatic Brain Injury in Mice
Published on: September 28, 2022
Gambogic amide, a selective TrkA agonist, does not improve outcomes from traumatic brain injury in mice
Maddison R Johnstone1, Mujun Sun2, Caroline J Taylor1
1a Department of Physiology, Anatomy and Microbiology , School of Life Sciences, La Trobe University , Melbourne , VIC , Australia.
Objectives:
There is evidence that treatment with nerve growth factor (NGF) may reduce neuroinflammation and apoptosis after a traumatic brain injury (TBI). NGF is thought to exert its effects via binding to either TrkA or p75 neurotrophin receptors. This study aimed to investigate the effects of a selective TrkA agonist, gambogic amide (GA), on TBI pathology and outcomes in mice following lateral fluid percussion injury.
Methods:
Male C57BL/6 mice were given either a TBI or sham injury, and then received subcutaneous injections of either 2 mg/kg of GA or vehicle at 1, 24, and 48 h post-injury. Following behavioural studies, mice were euthanized at 72 h post-injury for analysis of neuroinflammatory, apoptotic, and neurite outgrowth markers.
Results:
Behavioural testing revealed that GA did not mitigate motor deficits after TBI. TBI caused an increase in cortical and hippocampal expression of several markers of neuroinflammation and apoptosis compared to sham groups. GA treatment did not attenuate these increases in expression, possibly contributed to by our finding of TrkA receptor down-regulation post-TBI.
Conclusions:
These findings suggest that GA treatment may not be suitable for attenuating TBI pathology and improving outcomes.
