Régulation des récepteurs glutamatergiques dans différents modèles de vulnérabilité neuronale
Bibliographic record
Abstract
Throughout the years, the interest for Alzheimer's disease and diabetes has grown rapidly, especially with ageing of the population.Even thought the exact causes of the neuronal vulnerability observed during these pathology are stiil un known, we suggest that the cognitive disorders reported during these diseases might be related to the glutamatergic system, particularly to the regulation of AMPA and NMDA receptor.b verify this hypothesis, we examined whether brain glutamate receptors and long-term potentiation (LTP) were altered in the hippocampus ofapoli poprotein E (apoE) knock-out mice, a model ofAlzheimer's disease, as well as in non obese diabetic (NOD) mice, a genetic model of type I diabetes.Our electrophysiological analyses demonstrated that the LTP induced in the CAl hippocampal region by a theta-burst stimulation was lower for young apoE knock-out mice as well as for NOD mice.Moreover, this LTP defect in NOD mice was correlated to an increase in the N-méthyl-D-aspartate (NMDA) binding sites while it was associated to an impairment ofa-amino-3-hydroxy-5-m ethylisoxazole-4propionique (AMPA) receptor regulation by the lipid environment for the apoE knock-out mice.vi In order to understand the cellular mechanisms underlying glutamatergic te ceptor regulation, we studied the effect of different inositols, especially the D-myo inositol-(1,2,3,4,5,6) hexakisphosphate ( InsP6) which is one ofthe most abundant, on AMPA and MvIDA receptor properties.In this study, we demonstrated that InsP6 specifically regulates AMPA receptor distribution between synaptic and microsomal fraction by promoting an accumulation of these receptors into the synapse, an effect that could be regulated by clathrin-dependant mechanisms.Taken together, our resuits suggest that the cognitive disorders observed dur ing diabetes and Alzheimer's disease are associated to a modification of AIVWA and NMDA receptor regulation.furthermore, since inositol phosphate concentration is aftered in these pathologies and that InsP6 alters AIvWA receptor modulation, we pro pose that inositol could affect the glutamatergic system and thereby be involved in learning and memory.
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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) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.001 | 0.001 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.001 | 0.000 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.003 | 0.000 |
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".