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Microtubule-associated protein 2 levels decrease in hippocampus following traumatic brain injury
1Department of Neurosurgery, University of Texas Health Sciences Center, Houston.
Abstract:
We examined microtubule-associated protein 2 (MAP2) levels in hippocampal and cortical tissue 3 h following moderate traumatic brain injury (TBI) in the rat. MAP2 levels were assayed by quantitative immunoreactivity in tissue fractions obtained from naive, sham-injured, or fluid percussion-injured animals. Tissues were homogenized in the presence of protease inhibitors (0.3 mM phenylmethylsulfonyl fluoride, PMSF), a specific calpain inhibitors (0.1 mM leupeptin), and chelators (2 mM ethylene glycol-bis-tetraacetic acid, EGTA; 1 mM ethylenedinitrilo-tetraacetic acid, EDTA) to eliminate in vitro MAP2 proteolysis during tissue processing. Compared to naive rats, sham injury had no effect on soluble MAP2 levels in either cortex (105.0 +/- 4.4% of naive value) or hippocampus (106.6 +/- 5.2% of naive value). However, TBI caused a significant (p < 0.005) decrease in hippocampal MAP2 levels (55.7 +/- 5.9% of sham-injured controls). The effect appeared to be regionally selective, since the MAP2 decrease did not occur in cortex (89.1 +/- 1.4%). The degree of MAP2 decrease in hippocampus was similar in both membrane (57.8%) and cytosolic (55.7%) fractions, ruling out the possibility of partitioning artifacts. The data suggest that sublethal alterations of neuronal structure and function caused by MAP2 degradation may play an important role in the development of TBI-induced functional deficits. Since MAP2 is exclusively associated with the cytoskeleton in somal and dendritic compartments of neurons, the pathophysiology of sublethal magnitudes of TBI may also involve dendritic and somal dysfunction.
Insights
Traumatic brain injury (TBI) significantly reduces microtubule-associated protein 2 (MAP2) in the hippocampus, but not the cortex. This MAP2 degradation suggests neuronal dysfunction contributes to TBI deficits.
Area of Science:
- Neuroscience
- Cell Biology
- Trauma Research
Background:
- Microtubule-associated protein 2 (MAP2) is crucial for neuronal structure and function.
- Traumatic brain injury (TBI) can lead to significant neurological deficits.
Purpose of the Study:
- To investigate the impact of moderate TBI on MAP2 levels in rat hippocampus and cortex.
- To determine if MAP2 degradation plays a role in TBI-induced neuronal dysfunction.
Main Methods:
- Quantitative immunoreactivity was used to assay MAP2 levels in hippocampal and cortical tissue fractions.
- Rats were subjected to fluid percussion injury (TBI), sham injury, or left naive.
- Protease inhibitors and chelators were used during tissue processing to prevent in vitro MAP2 degradation.
Main Results:
- Sham injury had no significant effect on soluble MAP2 levels in either brain region.
- TBI caused a significant decrease in hippocampal MAP2 levels (55.7% of sham controls).
- MAP2 levels in the cortex remained largely unaffected by TBI (89.1% of sham controls), indicating regional selectivity.
Conclusions:
- TBI induces a significant, regionally selective decrease in hippocampal MAP2 levels.
- MAP2 degradation in the hippocampus suggests impaired neuronal structure and function contribute to TBI deficits.
- Dendritic and somal dysfunction may be involved in the pathophysiology of sublethal TBI.