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Activation of nicotinic α(7) acetylcholine receptor enhances long term potentation in wild type mice but not in APP(swe)/PS1ΔE9 mice

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  1. DNA methylation regulates CHRNA7 transcription and can be modulated by valproate

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  2. Increased oxidation of RNA despite reduced mitochondrial respiration after chronic electroconvulsive stimulation of rat brain tissue

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  3. Acetazolamide lowers intracranial pressure and modulates the cerebrospinal fluid secretion pathway in healthy rats

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  4. An oral NaV1.8 blocker improves motor function in mice completely deficient of myelin protein P0

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  5. Serotonergic projections from the raphe nuclei to the subthalamic nucleus; a retrograde- and anterograde neuronal tracing study

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  1. Sex-Related Differences in Outcomes of Alcohol Septal Ablation for Hypertrophic Obstructive Cardiomyopathy

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  2. Alcohol dose in septal ablation for hypertrophic obstructive cardiomyopathy

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  3. Anti-Inflammatory Effect of Alpha7 Nicotinic Acetylcholine Receptor Modulators on BV2 Cells

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Amyloid β (Aβ) plays a central role in Alzheimer's disease (AD) and binds to the nicotinic α(7) receptor (α(7) nAChR). Little is known about the degree to which the binding of Aβ to the α(7) nAChR influences the role of this receptor in long-term potentiation (LTP), however. We have studied the effect of the partial α(7) nAChR agonist SSR180711 on hippocampal slice preparations from normal wild type (Wt) and APP(swe)/PS1ΔE9 transgenic (Tg) mice. In the hippocampal slices from the 6 months old Wt mice, the application of both nicotine (5μM) and SSR180711 (300nM) resulted in a significant enhancement of LTP expressed in area CA1. However, in the Tg mice the application of SSR180711 did not result in an increase in LTP beyond control levels. The amount of binding of the α(7) nAChR ligand 125-I-α-bungarotoxin was not different between in Tg and Wt mice. These findings indicate that the α(7) nAChR is functionally blocked in the hippocampal neurons, downstream of the α(7) nAChR, and that this is likely due to an interaction between the receptor and Aβ, which leads to changes in LTP.
Original languageEnglish
JournalNeuroscience Letters
Volume487
Issue number3
Pages (from-to)325-9
Number of pages5
ISSN0304-3940
DOIs
Publication statusPublished - 2011

    Research areas

  • Amyloid beta-Protein Precursor, Animals, Bicyclo Compounds, Heterocyclic, Excitatory Postsynaptic Potentials, Female, Hippocampus, Humans, Long-Term Potentiation, Mice, Mice, Transgenic, Nicotine, Nicotinic Agonists, Organ Culture Techniques, RNA-Binding Proteins, Receptors, Nicotinic, Ribosomal Proteins

ID: 33247814