Chronic Loud Noise—Biochemical and Ultrastructural Alterations in Auditory and Limbic Regions of the Rat Brain

Chronic noise is an environmental risk factor leading to a number of pathologies at different levels of the organism, including the brain. The pathological changes induced by noise have been mainly studied in the regions of classical auditory system. However, neuroanatomy of sound processing is extremely complex as this process is supporting by not only classical auditory system, but brain regions outside the classical auditory pathways, including limbic areas. In the present study, we compare biochemical and ultrastructural alterations, provoked by 30 days’ loud noise in classical auditory and limbic regions of adult male rat brain: the central nucleus of inferior colliculus, basolateral amygdala and the hippocampus. We have shown that 30 days’ loud noise exposure leads to biochemical and ultrastructural alterations in these regions. Depending on the area, significant changes were demonstrated for the protein components of synaptic vesicles (synaptophysin), imflammosomes (AIM2 and NLRP3) and mitochondrial oxidative phosphorylation system (succinate dehydrogenase complex iron sulfur subunit B). Lipid oxidative degradation product - malondialdehyde protein adducts are significantly increased in the central nucleus of inferior colliculus. Some of these changes could be of a compensatory nature. The central nucleus of the inferior colliculus demonstrates moderate and severe ultrastructural alterations. The ultrastructure of limbic regions was more preserved. The data convincingly indicate the interrelated molecular and morphological changes after long-term loud noise exposure in classical auditory and limbic regions of the brain. Observed changes may lead to the pathological processes harming normal functioning of the brain