Research Paper Volume 11, Issue 7 pp 1934—1964
Ginsenoside Rb1 prevents MPTP-induced changes in hippocampal memory via regulation of the α-synuclein/PSD-95 pathway
- 1 Central Laboratory and Department of Neurology, Shunde Hospital, Southern Medical University (The First People’s Hospital of Shunde Foshan), Foshan 528300, China
- 2 Department of Traditional Chinese Medicine, Medical College, Xiamen University, Xiamen 361102, China
- 3 Teaching Center of Experimental Medicine, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China
- 4 Key Laboratory of Neuroscience, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China
- 5 Shenzhen Research Institute of Xiamen University, Shenzhen 518000, China
received: December 6, 2018 ; accepted: March 20, 2019 ; published: April 4, 2019 ;https://doi.org/10.18632/aging.101884
How to Cite
Copyright: Qu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Memory deficiency is a common non-motor symptom of Parkinson’s disease (PD), and conventionally, α-synuclein is considered to be an important biomarker for both motor and cognitive characteristics attributed to PD. However, the role of physiological α-synuclein in cognitive impairment remains undetermined. Ginsenoside Rb1 has been shown to protect dopaminergic neurons (DA) from death and inhibit α-synuclein fibrillation and toxicity in vitro. Our recent study also revealed that ginsenoside Rb1 ameliorates motor deficits and prevents DA neuron death via upregulating glutamate transporter GLT-1 in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. Whether Rb1 can improve memory deficiency and the underlying mechanism is still unknown. In this study, we found that Rb1 can prevent the spatial learning and memory deficits, increase long-term potentiation (LTP) and hippocampal glutamatergic transmission in the MPTP mouse model. The underlying neuroprotective mechanism of Rb1-improved synaptic plasticity involves Rb1 promoting hippocampal CA3 α-synuclein expression, restoring the glutamate in the CA3-schaffer collateral-CA1 pathway, and sequentially increasing postsynaptic density-95 (PSD-95) expression. Thus, we provide evidence that Rb1 modulates memory function, synaptic plasticity, and excitatory transmission via the trans-synaptic α-synuclein/PSD-95 pathway. Our findings suggest that Rb1 may serve as a functional drug in treating the memory deficiency in PD.
DG: dentate gyrus; LTP: long-term potentiation; mEPSCs: miniature excitatory postsynaptic currents; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; PSD-95: postsynaptic density-95.