Acrylamide neurotoxicity on the cerebrum of weaning rats

• Published in: Neural regeneration research Vol. 10; no. 6; pp. 938 - 943
• Main Authors: Tian, Su-Min, Ma, Yu-Xin, Shi, Jing, Lou, Ting-Ye, Liu, Shuai-Shuai, Li, Guo-Ying
• Format: Journal Article
• Language: English
• Published: India Medknow Publications and Media Pvt. Ltd 01.06.2015; Medknow Publications & Media Pvt. Ltd; School of Basic Medicine, Guangdong Pharmaceutical University, Guangzhou, Guangdong Province, China%Xiqiao People’s Hospital, Foshan, Guangdong Province, China%Clinical Laboratory of First Afifliated Hospital, Xinxiang Medical University, Xinxiang, Henan Province, China%Guangzhou University of Chinese Medicine, Guangzhou, Guangdong Province, China; Medknow Publications & Media Pvt Ltd; Wolters Kluwer Medknow Publications
• Subjects: 5-triphenyl-2H-tetrazolium chloride staining; Acrylamide; aging; animal model; axon; blood brain barrier; bone marrow mesenchymal stem cells; Brain; brain concussion; brain injury; brain-derived neurotrophic factor; Ca 2; cell therapy; cellular therapy; cerebral ischemia; cerebral ischemia/reperfusion injury; cerebrum; cognitive function; complications; cortex; curcumin; diagnosis; Drinking water; dual diagnosis; Eg5; enhanced susceptibility-weighted angiography image; Enzymes; excitatory postsynaptic potential; ferumoxytol; Food; glial fibrillary acidic protein; glutamate; glutamic acid decarboxylase; Health aspects; hippocampus; HIV-1 gp120 V3 loop; HIV-associated neurocognitive disorders; human adipose-derived stem cells; hydrogen sulfide; immunofluorescence; intracerebral injection; kinesin-5; Laboratory animals; long-term potentiation; magnetic resonance imaging; Medical research; microtubule; middle cerebral artery occlusion; modified neurological severity scores; molecular motor protein; monastrol; Morphology; MSCs; multiple sclerosis; myogenic differentiation; nanocarrier; Nerve degeneration; nerve regeneration; Nervous system; neural regeneration; neurite outgrowth; neurodegenerative disorders; neuroimaging; neuromuscular junction (NMJ); neurons; neuroplasticity; neuroprotection; Neurotoxicity; neurotrophic factor; non-invasive brain stimulation; NSFC grant; NSFC grants; organ index; output/input curve; P2X 7 receptor; paired-pulse facilitation; peptide library; phage display; plasticity; Polyclonal antibodies; post-concussion syndrome; protection; Prussian blue staining; rats; regeneration; rehabilitation; Risk factors; Schwann cells; sodium hydrosulfide; Software; spinal cord injuries; superparamagnetic iron oxide particles; synaptosome; tail vein injection; targeting; telomere shortening; TGF-β/BMP-7/Smad signaling; transcranial magnetic stimulation; traumatic brain injury; Trf3; tumor suppression; Weaning; γ-aminobutyric acid; γ-氨基丁酸; 丙烯酰胺; 免疫组织化学染色; 大脑皮层; 断奶大鼠; 毒性作用; 神经毒性; 谷氨酸脱羧酶; United States > US; China; cortex; cerebrum; neural regeneration; neurotoxicity; γ-aminobutyric acid; nerve regeneration; glial fibrillary acidic protein; glutamate; weaning; glutamic acid decarboxylase; organ index
• ISSN: 1673-5374; 1876-7958
• DOI: 10.4103/1673-5374.158357

The mechanism underlying acrylamide-induced neurotoxicity remains controversial. Previous studies have focused on acrylamide-induced toxicity in adult rodents, but neurotoxicity in weaning rats has not been investigated. To explore the neurotoxic effect of acrylamide on the developing brain, weaning rats were gavaged with 0, 5, 15, and 30 mg/kg acrylamide for 4 consecutive weeks. No obvious neurotoxicity was observed in weaning rats in the low-dose acrylamide group （5 mg/kg）. However, rats from the moderateand high-dose acrylamide groups （15 and 30 mg/kg） had an abnormal gait. Furthermore, biochemical tests in these rats demonstrated that glutamate concentration was significantly reduced, and ~-aminobutyric acid content was significantly increased and was dependent on acrylamide dose. Immunohis- tochemical staining showed that in the cerebral cortex, γ-aminobutyric acid, glutamic acid decarboxylase and glial fibrillary acidic protein expression increased remarkably in the moderate- and high-dose acrylamide groups. These results indicate that in weaning rats, acrylamide is positively associated with neurotoxicity in a dose-dependent manner, which may correlate with upregulation of γ-aminobutyric acid and subsequent neuronal degeneration after the initial acrylamide exposure.