Ginkgo biloba Extract Improves Dendritic Spine Injury in Cerebellar Purkinje Cells Induced by MPTP in Mice by Regulating the PLK2-SPAR Pathway.

IF 1.6 4区 医学 Q4 NEUROSCIENCES Synapse Pub Date : 2025-03-01 DOI:10.1002/syn.70013
Yilin Lyu, Yumei Zhang
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引用次数: 0

Abstract

Parkinson's disease (PD) is a common neurodegenerative disease, and, currently, there is no cure for patients with PD. Studies have shown that Ginkgo biloba extract (EGb) has good neuroprotective effects against PD. The cerebellum is widely involved in cognitive function and may be related to the regulation of static tremors in PD. However, research on the corresponding microstructures is limited. Purkinje cells (PCs) are the only efferent neurons present in the cerebellum, and dendritic spines in PCs are considered the key structures for transmitting neuronal excitatory signals. When neurons are activated, polo-like kinase 2 (PLK2) is expressed, leading to the degradation of spine-associated Rap guanosine triphosphatase activating protein (SPAR) and, ultimately, the loss of postsynaptic density protein 95 (PSD-95), causing changes in the morphology or quantity of dendritic spines. This raises the question of whether the neuroprotective effect of EGb involves the PLK2-SPAR pathway. In this study, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to establish a mouse model of dopamine neuronal injury. Golgi staining was performed to observe the dendritic spine changes. Immunohistochemistry was used to detect the expression of PLK2, SPAR, and PSD-95. The results showed that EGb improves MPTP-induced behavioral changes, dopamine neuronal injury, and dendritic spine damage in mice. In addition, EGb reversed the changes in PLK2, SPAR, and PSD-95 expressions caused by MPTP, revealing the potential mechanism by which EGb improves the condition of patients with PD.

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来源期刊
Synapse
Synapse 医学-神经科学
CiteScore
3.80
自引率
0.00%
发文量
38
审稿时长
4-8 weeks
期刊介绍: SYNAPSE publishes articles concerned with all aspects of synaptic structure and function. This includes neurotransmitters, neuropeptides, neuromodulators, receptors, gap junctions, metabolism, plasticity, circuitry, mathematical modeling, ion channels, patch recording, single unit recording, development, behavior, pathology, toxicology, etc.
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