| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2583326 | Environmental Toxicology and Pharmacology | 2013 | 7 Pages |
To investigate the toxic effects of high-speed railway noise on learning and memory function, Sprague-Dawley (SD) rats were exposed to high-speed railway noise for 90 days. The noise was recorded from an actual environment and adjusted to a day–night equivalent continuous A-weighted sound pressure level (Ldn) of 70 dB(A). Transmission electron microscopy (TEM) and Western blot analysis were used to observe the synaptic ultrastructure and detect the level of phosphorylated-Ca2+/calmodulin-dependent protein kinase II (p-CaMKII), respectively, in the hippocampus, temporal lobe and amygdala. Compared with the sham control group, the results of the TEM showed that the width of the noise model group's synaptic cleft increased markedly in the hippocampus, amygdala (P < 0.05) and temporal lobe (P < 0.01); the thickness of postsynaptic density (PSD) decreased significantly (P < 0.01). The results of the TEM suggest that the synaptic plasticity of structure and function were abnormal and that this abnormality resulted in a reduction in synaptic transmission efficiency. This reduction may have led to dysfunctions in learning and memory. Additionally, the Western blot analyses revealed that the level of p-CaMKII decreased significantly in the temporal lobe of the noise model group compared with the sham control group (P < 0.05). The results of the Western blot analysis indicate a reduction in synaptic transmission efficiency, which resulted in impairments in learning and memory function in the temporal lobe. Both of the above conclusions are consistent with each other.
Graphical abstractFigure optionsDownload full-size imageDownload as PowerPoint slideHighlights► The effects of high-speed railway noise on learning and memory function were investigated. ► Sprague-Dawley (SD) rats were exposed to 70 dB(A) high-speed railway noise for 90 days. ► The synaptic ultrastructure was observed in the hippocampus, temporal lobe and amygdala. ► The level of p-CaMKII was detected in the hippocampus, temporal lobe and amygdala.
