Abstract
Traumatic Brain Injury (TBI) is one of the most common causes of neurological damage in young populations. It has been previously suggested that one of the mechanisms that underlie brain injury is Axonal Outgrowth Inhibition (AOI) that is caused by altered composition of the gangliosides on the axon surface. In the present study, we have found a significant reduction of GM1 ganglioside levels in the cortex in a closed head traumatic brain injury model of a mouse, induced by a weight drop device. In addition, axonal regeneration in the brains of the injured mice was affected as seen by the expression of the axonal marker pNF-H and the growth cones (visualized by F-actin and β-III-tubulin). NeuN immunostaining revealed mTBI-induced damage to neuronal survival. Finally, as expected, spatial and visual memories (measured by the Y-maze and the Novel Object Recognition tests, respectively) were also damaged 7 and 30 days post injury. A single low dose of GM1 shortly after the injury (2 mg/kg; IP) prevented all of the deficits mentioned above. These results reveal additional insights into the neuroprotective characteristics of GM1 in prevention of biochemical, cellular and cognitive changes caused by trauma, and may suggest a potential intervention for mTBI.
Highlights
Traumatic Brain Injury (TBI) occurs when an object or external force hits the head
Our basic hypothesis refers to the alteration in ganglioside expression as one of the mechanisms that underlie the damage in the brains of Mild Traumatic Brain Injury (mTBI) mice
We evaluated the expression of GM1 using an Indirect enzyme-linked immunoassay (ELISA) test that revealed a significant reduction in GM1 content in the cortex of the injured mice 72 hrs post mTBI compared with control mice (21.08 ± 4.23 and 47.21 ± 8.7, respectively)
Summary
Traumatic Brain Injury (TBI) occurs when an object or external force hits the head. The main causes of injury are road accidents, falls, assaults, and sport injuries[1]. Cells may die an apoptotic or necrotic death immediately after injury Following these events, the secondary injury occurs within a period of hours to weeks after the first injury[8], which will initiate a series of inflammatory reactions. One of the suggested explanations is the axonal outgrowth inhibition (AOI), which occurs partly because of a change in the composition of the gangliosides on the axon surface and partly by the accumulation of axonal regeneration inhibitors (ARIs) at the site of the damage. This accumulation of proteins mainly involves Myelin-Associated-Glycoprotein (MAG), NOGO and Oligodendrocyte-Myelin glycoprotein (OMgp). It was shown that neither the impact of the blast nor the administration of GM1 ganglioside affected the GD1a ganglioside levels[18]
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