MPTP‐induced changes in hippocampal synaptic plasticity and memory are prevented by memantine through the BDNF‐TrkB pathway
Open accessAbstract
BACKGROUND AND PURPOSE: Mild cognitive deficit in early Parkinson's disease (PD) has been widely studied. Here we have examined the effects of memantine in preventing memory deficit in experimental PD models and elucidated some of the underlying mechanisms. EXPERIMENTAL APPROACHES: I.p. injection of 1-methyl-4- phenyl-1,2,3,6-tetrahydro pyridine (MPTP) in C57BL/6 mice was used to produce models of PD. We used behavioural tasks to test memory. In vitro, we used slices of hippocampus, with electrophysiological, Western blotting, real time PCR, elisa and immunochemical techniques. KEY RESULTS: Following MPTP injection, long-term memory was impaired and these changes were prevented by pre-treatment with memantine. In hippocampal slices from MPTP treated mice, long-term potentiation (LTP) -induced by θ burst stimulation (10 bursts, 4 pulses) was decreased, while long-term depression (LTD) induced by low-frequency stimulation (1 Hz, 900 pulses) was enhanced, compared with control values. A single dose of memantine (i.p., 10 mg·kg(-1) ) reversed the decreased LTP and the increased LTD in this PD model. Activity-dependent changes in tyrosine kinase receptor B (TrkB), ERK and brain-derived neurotrophic factor (BDNF) expression were decreased in slices from mice after MPTP treatment. These effects were reversed by pretreatment with memantine. Incubation of slices in vitro with 1-methyl-4-phenylpyridinium (MPP(+) ) decreased depolarization-induced expression of BDNF. This effect was prevented by pretreatment of slices with memantine or with calpain inhibitor III, suggesting the involvement of an overactivated calcium signalling pathway. CONCLUSIONS AND IMPLICATIONS: Memantine should be useful in preventing loss of memory and hippocampal synaptic plasticity in PD models.
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BDNF treatment of brain slices from MPTP-treated mice was able to restore the impaired synaptic plasticity.
“Moreover, BDNF treatment of brain slices from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice was able to restore the impaired synaptic plasticity [102].”
From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [102]
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BDNF as a Promising Therapeutic Agent in Parkinson’s Disease
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- Authors
- Zhu, G., Li, J., He, L., Wang, X., & Hong, X.
- Affiliations
- Anhui University of Traditional Chinese Medicine (CN)
- Western University of Health Sciences (US)
- Corresponding author
- Zhu, Guoqi
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2015-03-26
- Volume
- 172
- Issue
- 9
- Pages
- 2354-2368
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC4403099
- OpenAlex
- W1587866768
- Cited by
- 118
- References
- 61
- Citations by year
- 2026: 2 · 2025: 10 · 2024: 10 · 2023: 11 · 2022: 11 · 2021: 10 · 2020: 12 · 2019: 15 · 2018: 8 · 2017: 16 · 2016: 11 · 2015: 2
- FWCI
- 8.70
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Anhui University
- Natural Science Foundation of Anhui Province (1308085QH135)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- memantine, Parkinson's disease, MPTP, hippocampal synaptic plasticity, memory impairment, BDNF/TrkB pathway, long-term potentiation, long-term depression, ERK, MPP+, calpain, calcium signaling, neuroprotection
- MeSH terms
- Animals, Antiparkinson Agents, Behavior, Animal, Disease Models, Animal, Hippocampus, Male, Memantine, Membrane Glycoproteins, Memory Disorders, Mice, Inbred C57BL, Neuronal Plasticity, Protein-Tyrosine Kinases, Synapses, Time Factors, Signal Transduction, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, 1-Methyl-4-phenylpyridinium, Brain-Derived Neurotrophic Factor, Calcium Signaling, Parkinsonian Disorders, Receptor, trkB, Extracellular Signal-Regulated MAP Kinases, Memory, Long-Term, In Vitro Techniques
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