Impulse noise exposure in rats causes cognitive deficits and changes in hippocampal neurotransmitter signaling and tau phosphorylation

Noise exposure has been characterized as a stressor, and its non-auditory effects on the central nervous system have been established both epidemiologically and experimentally. Little is known about the impact of impulse noise on the brain, however. In this study, we examined the effects of impulse noise stress on spatial learning and memory and on associated changes in the hippocampus. Rats were exposed to 20 sound impulses with a peak sound pressure of 165 dB and duration of 100 ms. Impulse noise stress led to a temporary decrease in cognitive function as evidenced by poor spatial memory in the Morris water maze (MWM). Effects of noise on the glutamate (Glu)–N-methyl-d-aspartic acid receptor (NMDAR) signaling system and hippocampal tau phosphorylation were investigated by high performance liquid chromatography, Western blotting, and immunohistochemistry. The concentrations of Glu and aspirate (Asp) in the hippocampus were increased at 30 min after exposure and remained elevated for the entire observation period (24 h), while the content of glycine (Gly) was stable for several hours following noise but also increased by 24 h after noise stress. Impulse noise stress also caused a significant increase in NMDAR 2B subunit (NR2B) expression and a two-phase increase in tau phosphorylation in hippocampus. Immunohistochemistry confirmed tau hyperphosphorylation in hippocampus that was most prominent in the dentate gyrus (DG) and CA1 region. These findings demonstrate that impulse noise stress impairs early spatial memory, possibly by disrupting Glu-NMDAR signaling and triggering aberrant tau hyperphosphorylation in hippocampus.

► Impulse noise exposure caused spatial memory impairments in rats.
► Impulse noise exposure altered amino acid neurotransmitter levels in the hippocampus.
► Impulse noise exposure induced elevated expression of NR2B in the hippocampus.
► Impulse noise exposure caused tau hyperphosphorylation in the hippocampus.