Primary Blast-Induced Changes in Akt and GSK3β Phosphorylation in Rat Hippocampus
Bibliographic record
Abstract
Traumatic brain injury (TBI) due to blast from improvised explosive devices (IEDs) has been a leading cause of morbidity and mortality in recent conflicts in Iraq and Afghanistan. However, the mechanisms of primary blast-induced TBI are not well understood. In the present study, the effects of simulated primary blast wave on the phosphorylation status of Akt and its downstream effector kinase, glycogen synthase kinase 3β (GSK3β), in rat hippocampus were investigated. Male Sprague-Dawley (SD) rats (350 – 400 g) were exposed to a single pulse shock wave (25 psi; ~7 msec duration) and sacrificed 1 day, 1 week, or 6 weeks after exposure. Total and phosphorylated Akt, as well as phosphorylation of its down-stream effector kinase GSK3β (at serine 9) were detected with western blot analysis and immunohistochemistry. Results showed that Akt phosphorylation at serine 473 was dramatically increased 1 day after blast on the ipsilateral side of the hippocampus, and this elevation persisted until at least 6 weeks post exposure. Similarly, phosphorylation of GSK3β at serine 9, which inhibits GSK3β activity, was also increased starting at 1 day and persisted until at least 6 weeks after primary blast on the ipsilateral side. In contrast, p-Akt was increased 1 week and 6 weeks on the contralateral side, while p-GSK3β was increased 1 day and 1 week after primary blast exposure. No significant changes in total protein levels of Akt and GSK were observed on either side of the hippocampus at any time points. Immunohistochemical results showed that increased p-Akt was mainly of neuronal origin in the CA1 region of the hippocampus and once phosphorylated, was translocated to the dendritic membranes of the same neurons. Finally, electrophysiological data showed that evoked synaptic N-methyl-D-aspartate (NMDA) receptor activity was significantly increased 6 weeks after primary blast, suggesting that the increased Akt phosphorylation observed in this study may be a result of enhanced synaptic NMDA receptor activation, or wise versa.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.003 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".