Neural Regeneration Research (Jan 2015)
Acrylamide neurotoxicity on the cerebrum of weaning rats
- Su-min Tian,
- Yu-xin Ma,
- Jing Shi,
- Ting-ye Lou,
- Shuai-shuai Liu,
- Guo-ying Li
Affiliations
- Su-min Tian
- Yu-xin Ma
- Jing Shi
- Ting-ye Lou
- Shuai-shuai Liu
- Guo-ying Li
- DOI
- https://doi.org/10.4103/1673-5374.158357
- Journal volume & issue
-
Vol. 10,
no. 6
pp. 938 – 943
Abstract
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 moderate- and 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 γ-aminobutyric acid content was significantly increased and was dependent on acrylamide dose. Immunohistochemical 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.
Keywords
- microtubule
- axon
- kinesin-5
- Eg5
- regeneration
- monastrol
- molecular motor protein
- aging
- neurodegenerative disorders
- telomere shortening
- MSCs
- cellular therapy
- traumatic brain injury
- spinal cord injuries
- dual diagnosis
- diagnosis
- complications
- rehabilitation
- post-concussion syndrome
- brain concussion
- blood brain barrier
- phage display
- peptide library
- nanocarrier
- targeting
- Schwann cells
- neurite outgrowth
- neuromuscular junction (NMJ)
- multiple sclerosis
- TGF-β/BMP-7/Smad signaling
- myogenic differentiation
- Trf3
- tumor suppression
- nerve regeneration
- bone marrow mesenchymal stem cells
- cerebral ischemia
- tail vein injection
- middle cerebral artery occlusion
- cell therapy
- neuroprotection
- nerve regeneration
- brain injury
- neuroimaging
- ferumoxytol
- superparamagnetic iron oxide particles
- human adipose-derived stem cells
- middle cerebral artery occlusion
- intracerebral injection
- magnetic resonance imaging
- enhanced susceptibility-weighted angiography image
- modified neurological severity scores
- rats
- Prussian blue staining
- neural regeneration
- neural regeneration
- non-invasive brain stimulation
- transcranial magnetic stimulation
- neurotrophic factor
- brain-derived neurotrophic factor
- neuroplasticity
- hippocampus
- aging
- cognitive function
- nerve regeneration
- curcumin
- neurons
- HIV-1 gp120 V3 loop
- plasticity
- HIV-associated neurocognitive disorders
- output/input curve
- long-term potentiation
- excitatory postsynaptic potential
- paired-pulse facilitation
- Ca 2+
- synaptosome
- NSFC grants
- neural regeneration
- nerve regeneration
- brain injury
- hydrogen sulfide
- cerebral ischemia/reperfusion injury
- P2X 7 receptor
- 2
- 3
- 5-triphenyl-2H-tetrazolium chloride staining
- animal model
- protection
- sodium hydrosulfide
- immunofluorescence
- middle cerebral artery occlusion
- NSFC grant
- neural regeneration
- nerve regeneration
- γ-aminobutyric acid
- glial fibrillary acidic protein
- glutamic acid decarboxylase
- neurotoxicity
- weaning
- organ index
- cerebrum
- cortex
- glutamate
- neural regeneration