Effects of chronic noise on mRNA and protein expression of CRF family molecules and its relationship with p-tau in the rat prefrontal cortex

• Noise stress impacts the corticotropin-releasing factor (CRF) system.
• A chronic noise stress model was established to study rat prefrontal cortex (PFC).
• Chronic noise elevated plasma corticosterone and the CRF system in the PFC.
• Phosphorylated-tau and CRF co-localized to PFC neurons.
• This study links noise stress, CRF, and Alzheimer's disease-like changes in the PFC.

Chronic noise exposure has been associated with Alzheimer's disease (AD)-like pathological changes, such as tau hyperphosphorylation and β-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 (95 dB sound pressure level white noise, 4 h/day × 30 days). Chronic noise significantly accelerated the progressive overproduction of corticosterone and upregulated CRF and CRFR1 mRNA and protein, both of which persisted 7–14 days after noise exposure. In contrast, CRFR2 was elevated 3–7 days 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.