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1.
J Neurol Sci ; 368: 307-13, 2016 Sep 15.
Article in English | MEDLINE | ID: mdl-27538655

ABSTRACT

Chronic noise exposure has been associated with Alzheimer's disease (AD)-like pathological changes, such as tau hyperphosphorylation and ß-amyloid peptide accumulation in the prefrontal cortex (PFC). Corticotropin-releasing factor (CRF) is the central driving force in the stress response and a regulator of tau phosphorylation via binding to CRF receptors (CRFR). Little is known about the CRF system in relation to noise-induced AD-like changes in the PFC. The aim of this study was to explore the effects of chronic noise exposure on the CRF system in the PFC of rats and its relationship to tau phosphorylation. Male Wistar rats were randomly divided into control and noise exposure groups. The CRF system was evaluated following chronic noise exposure (95dB sound pressure level white noise, 4h/day×30days). Chronic noise significantly accelerated the progressive overproduction of corticosterone and upregulated CRF and CRFR1 mRNA and protein, both of which persisted 7-14days after noise exposure. In contrast, CRFR2 was elevated 3-7days following the last stimulus. Double-labeling immunofluorescence co-localized p-tau with CRF in PFC neurons. The results suggest that chronic noise exposure elevates the expression of the CRF system, which may contribute to AD-like changes.


Subject(s)
Corticotropin-Releasing Hormone/genetics , Corticotropin-Releasing Hormone/metabolism , Noise/adverse effects , Prefrontal Cortex/metabolism , RNA, Messenger/metabolism , Receptors, Corticotropin-Releasing Hormone/genetics , Receptors, Corticotropin-Releasing Hormone/metabolism , tau Proteins/metabolism , Acoustic Stimulation/methods , Animals , Corticosterone/blood , Disease Models, Animal , Enzyme-Linked Immunosorbent Assay , Gene Expression Regulation/physiology , Male , Rats , Rats, Wistar , Stress, Psychological/etiology , Stress, Psychological/metabolism , Time Factors
2.
Article in Chinese | MEDLINE | ID: mdl-27255049

ABSTRACT

OBJECTIVE: To study the effect of nano-SiO2 on spatial learning and memory. METHODS: Twenty-four male rats were randomly divided into 3 groups: control group (C group), low dose group (L group) and high dose group (H group). The rats were intragastrically administrated with nanometer particles at 25 and 100 mg/kg body weight every day for 4 weeks. After exposure, the ability of learning and memory of rats was tested by Morris water maze, and electrophysiological brain stereotactic method was used to test long-tear potentiation (LTP) in dentate gyrus (DG) of the rats. RESULTS: The increase rate of body weight in H group was reduced significantly compared with C group ( P < 0.05). In the space exploration experiment of Morris water maze test, the escape latency of H group was longer than that of C group (P < 0.05). The rats of H group spent less time in finding the target quadrant (P < 0.05) . The rate of LP induction of H group was significantly lower than that of C group (P < 0.05). After high fre quency stimulation (HFS), The changes of amplitude of population spike (PS) of L group and H group were lower than those of C group significantly (P < 0.05, P < 0.01). CONCLUSION: Nano-SiO2may result in impairment of spatial learning and memory ability by reducing the rate of LTP induction and the increase of PS in hippocampus.


Subject(s)
Dentate Gyrus/drug effects , Long-Term Potentiation/drug effects , Memory/drug effects , Nanoparticles/adverse effects , Silicon Dioxide/adverse effects , Spatial Learning/drug effects , Animals , Male , Maze Learning/drug effects , Rats
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