Soluble Aβ Oligomers Impair Dipolar Heterodendritic Plasticity by Activation of mGluR in the Hippocampal CA1 Region
| Autor: | Jianhua Zhao, Dennis J. Selkoe, Yifan Dang, Shaomin Li, Molly M Rajsombath, Anna Li |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Multidisciplinary Homosynaptic plasticity Chemistry musculoskeletal neural and ocular physiology Neurodegeneration Stimulation Long-term potentiation Hippocampal formation medicine.disease 03 medical and health sciences Basal (phylogenetics) 030104 developmental biology 0302 clinical medicine nervous system Metabotropic glutamate receptor Cellular neuroscience medicine lcsh:Q lcsh:Science Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | iScience, Vol 6, Iss, Pp 138-150 (2018) |
| ISSN: | 2589-0042 |
| Popis: | Summary: Soluble Aβ oligomers (oAβs) contribute importantly to synaptotoxicity in Alzheimer disease (AD), but the mechanisms related to heterogeneity of synaptic functions at local circuits remain elusive. Nearly all studies of the effects of oAβs on hippocampal synaptic plasticity have only examined homosynaptic plasticity. Here we stimulated the Schaffer collaterals and then simultaneously recorded in stratum radiatum (apical dendrites) and stratum oriens (basal dendrites) of CA1 neurons. We found that the apical dendrites are significantly more vulnerable to oAβ-mediated synaptic dysfunction: the heterosynaptic basal dendritic long-term potentiation (LTP) remained unchanged, whereas the homosynaptic apical LTP was impaired. However, the heterosynaptic basal dendritic plasticity induced by either spaced 10-Hz bursts or low-frequency (1-Hz) stimulation was disrupted by oAβs in a mGluR5-dependent manner. These results suggest that different firing patterns in the same neurons may be selectively altered by soluble oAβs in an early phase of AD, before frank neurodegeneration. : Neuroscience; Cellular Neuroscience; Disease Subject Areas: Neuroscience, Cellular Neuroscience, Disease |
| Databáze: | OpenAIRE |
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