Details

Autor(en) / Beteiligte

• ZHANG, Bin
• SHAO, Hua
• WANG, Xiu Hui
• CHEN, Xiao
• LI, Zhong Sheng
• CAO, Peng
• ZHU, Dan
• YANG, Yi Guang
• XIAO, Jing Wei
• LI, Bin

Titel

Acrylamide-induced Subacute Neurotoxic Effects on the Cerebral Cortex and Cerebellum at the Synapse Level in Rats

Ist Teil von

• Biomedical and environmental sciences, 2017-06, Vol.30 (6), p.432-443

Ort / Verlag

China: Elsevier B.V

Erscheinungsjahr

2017

Quelle

Access via ScienceDirect (Elsevier)

Beschreibungen/Notizen

• Objective To investigate acrylamide （ACR）-induced subacute neurotoxic effects on the central nervous system （CNS） at the synapse level in rats. Methods Thirty-six Sprague Dawley （SD） rats were randomized into three groups, （1） a 30 mg/kg ACR-treated group, （2） a 50 mg/kg ACR-treated group, and （3） a normal saline （NS）-treated control group. Body weight and neurological changes were recorded each day. At the end of the test, cerebral cortex and cerebellum tissues were harvested and viewed using light and electron microscopy. Additionally, the expression of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were investigated. Results The 50 mg/kg ACR-treated rats showed a significant reduction in body weight compared with untreated individuals （P 〈 0.05）. Rats exposed to ACR showed a significant increase in gait scores compared with the NS control group （P 〈 0.05）. Histological examination indicated neuronal structural damage in the 50 mg/kg ACR treatment group. The active zone distance （AZD） and the nearest neighbor distance （NND） of synaptic vesicles in the cerebral cortex and cerebellum were increased in both the 30 mg/kg and 50 mg/kg ACR treatment groups. The ratio of the distribution of synaptic vesicles in the readily releasable pool （RRP） was decreased. Furthermore, the expression levels of Synapsin I and P-Synapsin I in the cerebral cortex and cerebellum were decreased in both the 30 mg/kg and 50 mg/kg ACR treatment groups. Conclusion Subacute ACR exposure contributes to neuropathy in the rat CNS. Functional damage of synaptic proteins and vesicles may be a mechanism of ACR neurotoxicity.