Effects of vasoactive intestinal peptide on synapse of MPTP-induced mice with Parkinson&rsquo;s disease

Lü E* FEI Xue-chao LI Kan ZHAN Tong-xia LI Feng-jie FU Wen-yu*

doi:10.16098/j.issn.0529-1356.2018.01.005

PDF(626 KB)

Acta Anatomica Sinica ›› 2018, Vol. 49 ›› Issue (1) : 29-34. DOI: 10.16098/j.issn.0529-1356.2018.01.005

Neurobiology

Effects of vasoactive intestinal peptide on synapse of MPTP-induced mice with Parkinson’s disease

Lü E^1* FEI Xue-chao² LI Kan³ZHAN Tong-xia⁴ LI Feng-jie⁵ FU Wen-yu ^1*

Author information +

History +

Abstract

Objective To study the effects of vasoactive intestinal peptide (VIP) on synaptic and behavioral alterations in the mice model of Parkinson’s disease (PD) induced by 1-methyl-4-phenyl-1,2,3,6tetrahydropyridine (MPTP). Methods Thirty male C57BL/6 J mice were randomly divided into normal saline (NS) group, MPTP group and MPTP + VIP group. The behavioral changes of mice were measured by the Tru Scan system. The expression of tyrosine hydroxylase (TH) in the substantia nigra (SN) and striatum and vesicle-associated membrane protein 2 (VAMP2) and synapsin 1 (SYN1) in the striatum were examined by immunohistochemistry, and the levels of VAMP2 and SYN1 were analyzed by Western blotting. The synaptic structural changes in the SN were observed by transmission electron microscopy. Results In the behavioral test, the MPTP group had a significantly lower vertical movement distance than that of the control group, while the MPTP group was markedly higher than that of MPTP group. Compared with the MPTP group, VIP treatment obviously increased the average absorbance (AA) of TH, VAMP2 and SYN1 immunolabeling in striatum and the number of dopaminergic neurons in the SN, while the levels of the VAMP2 and SYN1 proteins also elevated. Synapse density in the model group was less than that in the control group. The amount of synaptic vesicles was decreased in the model group compared to the control, but normalized in the MPTP + VIP group. Conclusion VIP administration can up-regulate the expression of VAMP2 and SYN1, mitigate synaptic damage, protect dopaminergic neurons and improve movement in the MPTP model mice.

Key words

Parkinson’s disease / Vasoactive intestinal peptide / Vesicle-associated membrane protein 2 / Synapsin 1 / Western blotting / Transmission electron microscopy / Mouse

Cite this article

EndNote

Ris (Procite)

Bibtex

Download Citations

Lü E FEI Xue-chao LI Kan ZHAN Tong-xia LI Feng-jie FU Wen-yu. Effects of vasoactive intestinal peptide on synapse of MPTP-induced mice with Parkinson’s disease[J]. Acta Anatomica Sinica. 2018, 49(1): 29-34 https://doi.org/10.16098/j.issn.0529-1356.2018.01.005

References

［1］Sheng JS. Dysfunction of synaptic vesicle recycling and Parkinson’s disease［J］. Chemistry of Life, 2014, 3(2): 200-206. (in Chinese)

盛建松. 突触囊泡循环障碍与帕金森病［J］. 生命的化学, 2014, 34(2): 200-206.

［2］Morell M, Souza-Moreira L, González-Rey E. VIP in neurological diseases: more than a neuropeptide ［J］. Endocr Metab Immune Disord Drug Targets, 2012, 12(4):323-332.

［3］Zhuang WX, Liu ZY, Wang XJ, et al. Effects of vasoactive intestinal peptide on the activation of glia and the expression of associated inflammatory factors in the substantia nigra of Parkinson's disease rat models［J］. Acta Anatomica Sinica, 2016, 47(2): 178-184. (in Chinese)

庄文欣, 刘宗昱, 王雪净, 等. 血管活性肠肽对帕金森病大鼠黑质胶质细胞活化及相关炎性因子释放的影响［J］. 解剖学报, 2016, 47(2): 178-184.

［4］Yelkenli IH, Ulupinar E, Korkmaz OT, et al. Modulation of corpus striatal neurochemistry by astrocytes and vasoactive intestinal peptide (VIP) in Parkinsonian rats［J］. J Mol Neurosci, 2016, 59(2): 280-289.

［5］García E, Santana-Martínez R, Silva-Islas CA, et al. S-allyl cysteine protects against MPTP-induced striatal and nigral oxidative neurotoxicity in mice: participation of Nrf2［J］. Free Radic Res, 2014, 48(2): 159-167.

［6］Delgado M, Ganea D.Neuroprotective effect of vasoactive intestinal peptide (VIP) in a mouse model of Parkinson’s disease by blocking microglial activation［J］. FASEB J, 2003,17(8): 944-956.

［7］Lü E, Deng J, Yu Y, et al. Nrf2-ARE signals mediated the anti-oxidative action of electroacupuncture in an MPTP mouse model of Parkinson’s disease［J］. Free Radic Res, 2015, 49(11): 1296-1307.

［8］Lü E, Fu WY, Zhuang BX, et al. Changes of neurotransmitters in the brain of unilateral 6-OHDA-treated rat model with Parkinson’s disease［J］. Chinese Journal of Anatomy, 2008, 31(4): 541-544. (in Chinese)

吕娥, 付文玉, 庄宝祥, 等. 6-羟多巴胺制备的帕金森病大鼠脑内神经递质的变化［J］. 解剖学杂志, 2008, 31(4): 541-544.

［9］Lepeta K, Lourenco MV, Schweitzer BC, et al. Synaptopathies: synaptic dysfunction in neurological disorders A review from students to students［J］. J Neurochem, 2016, 138(6): 785-805.

［10］Stauch KL, Villeneuve LM, Purnell PR, et al. Loss of Pink1 modulates synaptic mitochondrial bioenergetics in the rat striatum prior to motor symptoms: concomitant complex I respiratory defects and increased complex Ⅱ-mediated respiration［J］. Proteomics Clin Appl, 2016, 10(12):1205-1217.

［11］Cochiolo JA, Ehsanian R, Bruck DK. Acute ultrastructural effects of MPTP on the nigrostriatal pathway of the C57BL/6 adult mouse: evidence of compensatory plasticity in nigrostriatal neurons［J］. J Neurosci Res, 2000, 59(1): 126-135.

［12］Jahn R, Scheller RH. SNAREs-engines for membrane fusion［J］. Nat Rev Mol Cell Biol, 2006, 7(9): 631-643.

［13］Barak B, Okun E, Ben-Simon Y, et al. Neuron-specific expression of tomosyn1 in the mouse hippocampal dentategyrus impairs spatial learning and memory［J］. Neuromolecular Med, 2013, 15(2): 351-363.

［14］Brunger AT, Weninger K, Bowen M, et al. Single-molecule studies of the neuronal SNARE fusion machinery［J］. Annu Rev Biochem, 2009, 78: 903-928.

［15］Gui W,Yu ChY,Wang K, et al. The effects of TNF-β1 on neuronal dendritic growth and the expression of synapsin1［J］. Journal of Apoplexy and Nervous Diseases, 2011, 28(10): 25-28. (in Chinese)

桂韦, 余传勇, 汪凯, 等. 转化生长因子β-1对神经元树突生长以及突触素1表达的影响［J］. 中风与神经疾病杂志, 2011, 28(10): 25-28.

［16］Lian T,Zhang LL,Li ZhY.Expression of synaptophsin in a developmental hippocampus of hypothyroid rats［J］. Chinese Journal of Endocrinology and Metabolism, 2007, 23(1): 72-74. (in Chinese)

练涛, 张丽丽, 李昭英. 突触体素在甲状腺功能减退大鼠脑海马发育期的表达［J］. 中华内分泌代谢杂志, 2007, 23(1): 72-74. 

［17］Reddy PH, Mani G, Park BS, et al. Differential loss of synaptic proteins in Alzheimer’s disease: implications for synaptic dysfunction［J］. Alzheimers Dis, 2005, 7(2): 103-117.

［18］Zeng HC, Li YY, Zhang L, et al. Prenatal exposure to perfluorooctanesulfonate in rat resulted in long-lasting changes of expression of synapsins and synaptophysin［J］. Synapse, 2011, 65(3): 225-233.