Chronic Loud Noise—Biochemical and Ultrastructural Alterations in Auditory and Limbic Regions of the Rat Brain
Abstract
Chronic noise is a major environmental risk factor leading to a number of pathologies in different parts of organisms, with a profound impact on health. The auditory system is the most vulnerable to the damaging effects of noise. However, sound processing is also supported by brain regions outside the classical auditory pathways, including limbic areas. Little is known about molecular and structural mechanisms of long-term noise effects in the limbic area. The work was aimed at filling this gap. In the present study, we compare biochemical and ultrastructural alterations, elicited by 30 days of loud noise in the classical auditory and limbic regions of adult male rat brain: the central nucleus of inferior colliculus, the basolateral amygdala and the hippocampus. We have shown that 30 days of' loud noise exposure leads to biochemical and ultrastructural alterations in these regions. Depending on the area, significant and specific changes were demonstrated for the protein components of synaptic vesicles, inflammasomes, and the mitochondrial oxidative phosphorylation system. The lipid oxidative degradation product, malondialdehyde protein adducts are significantly increased in the central nucleus of inferior colliculus. Some of these changes could be compensatory. The central nucleus of the inferior colliculus demonstrates moderate and severe ultrastructural alterations, whereas the ultrastructure of the limbic regions was more preserved. The data convincingly indicate the interrelated molecular and morphological changes after long-term loud noise exposure in the classical auditory and limbic regions of the brain. The observed changes may lead to pathological processes that harm the normal functioning of the brain.
Fields of Study & Subjects
Noise Effects and Management
Publication details
- Journal / source
- BioMed Research International
- Volume
- 2026
- Issue
- 1
- Pages
- e2680036–e2680036
- Publication date
- 1 January 2026
- Language
- EN