Acute high-intensity noise exposure exacerbates anxiety-like behavior via neuroinflammation and blood brain barrier disruption of hippocampus in male rats.

Abstract

The health risks associated with acute noise exposure are increasing, particularly the risk of mental health. This study aims to identify the association between acute high-intensity noise exposure and anxiety behavior in male rats, and to explore the associated neurobiological mechanisms. Male rats were subjected to different levels of acute high-intensity noise to determine the intensity that causes long-lasting anxiety-like behaviors. Anxiety-like behaviors were evaluated using the open field test (OFT) and the elevated plus maze test (EPMT) on the third day and 1month post-exposure, respectively. A range of techniques, including immunofluorescence staining, western blot, ELISA, and real-time quantitative PCR, were used to investigate neuronal apoptosis, glial cell activation, neuroinflammation, and blood-brain barrier (BBB) disruption in the hippocampus. Upon exposure to 135 dB of acute noise, male rats exhibited enduring anxiety-like behaviors. Subsequent investigations discovered that this noise intensity not only activated glial cells and triggered neuroinflammation within the hippocampus but also decreased the expression levels of ZO-1, claudin-5, and occludin, suggesting a disruption of the BBB. Additionally, this exposure was associated with the induction of neuronal apoptosis in the hippocampal region. In conclusion, acute exposure to 135 dB noise may cause persistent anxiety in male rats through a cyclical interaction between neuroinflammation and BBB disruption, potentially leading to neuronal apoptosis.