No hippocampal neuron or synaptic bouton loss in learning-impaired aged β-Amyloid precursor protein-null mice
| Autor: | Mathias Jucker, Hans-Peter Lipp, Michael E. Calhoun, H. Zheng, David P. Wolfer, Amie L. Phinney |
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| Rok vydání: | 1999 |
| Předmět: |
Aging
Presynaptic Terminals Synaptogenesis Morris water navigation task Cell Count Hippocampal formation Hippocampus Amyloid beta-Protein Precursor Mice Memory mental disorders medicine Amyloid precursor protein Animals Learning Maze Learning Swimming Mice Knockout Neurons Thigmotaxis Behavior Animal biology Learning Disabilities General Neuroscience Dentate gyrus medicine.disease medicine.anatomical_structure nervous system biology.protein Neuron Alzheimer's disease Psychology Neuroscience |
| Zdroj: | Neuroscience. 90:1207-1216 |
| ISSN: | 0306-4522 |
| DOI: | 10.1016/s0306-4522(98)00645-9 |
| Popis: | Aged beta-amyloid precursor protein-null mice were used to investigate the relationship between beta-amyloid precursor protein, hippocampal neuron and synaptic bouton number, and cognitive function. Learning and memory performance of aged beta-amyloid precursor protein-null mice and age-matched controls were assessed in the Morris water maze. Beta-amyloid precursor protein-null mice demonstrated impaired task acquisition as measured by significantly longer swim path lengths, a higher percentage of failed trials, and more frequent thigmotaxis behavior than controls. In a subsequent probe trial, beta-amyloid precursor protein-null mice spent significantly less time in the old goal quadrant, and made fewer crossings over the old platform location than did controls. No differences in motor or visual skills were observed which could account for the performance differences. In light of these findings and previous evidence for a role of beta-amyloid precursor protein in neuronal maintenance and synaptogenesis, we pursued the hypothesis that the learning impairment of beta-amyloid precursor protein-null mice may be a reflection of differences in neuron or synaptophysin-positive presynaptic bouton number. Thus, unbiased stereological analysis was used to estimate neuron and synaptic bouton number in dentate gyrus and hippocampal CA1 of the behaviorally characterized mice. No difference in neuron or synaptophysin-positive presynaptic bouton number was found between the beta-amyloid precursor protein-null mice and age-matched controls. Our results suggest that the learning impairment of beta-amyloid precursor protein-null mice is not mediated by a loss of hippocampal neurons or synaptic boutons. |
| Databáze: | OpenAIRE |
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