Calcium-Binding Proteins and Melatonin Receptors in the Central Auditory System of Aged Rats.

INTRODUCTION

Age-related hearing loss (ARHL) is a multifactorial disorder due to impairment in the peripheral or central auditory pathway (CAP). CAP impairment refers to difficulties in speech understanding, particularly in the presence of background noise, problems in discrimination, and integrating and separating binaural auditory information. Changes in CAP mechanisms, such as neurotransmitters or ion movement, may correlate with this impairment. The regulation of calcium (Ca2+) concentrations by Ca2+-binding proteins (CaBPs) is critical for synaptic function and plasticity, and changes are directly related to ARHL. Thus, changes in the neuronal expression of CaBPs in aging could be related to CAP disorders. Considering that supplementation with antioxidant and/or neuroprotective substances can delay neuronal loss in aging, antioxidant-based therapies can prevent and/or reduce the progression of ARHL in animal models and humans. The hormone melatonin has important antioxidant and neuroprotective actions, which can sometimes depend on melatonin receptors. This work aimed to investigate changes in the expression of CaBPs and melatonin receptors in the CAP stations and whether this expression could vary with aging.

METHODS

Brain sections of Wistar rats young and elderly were processed using immunohistochemistry technique, and for analysis and quantification, the stereology and optical density technique were used.

RESULTS

The analysis revealed a lower density of CaBP-immunoreactive cells in most CAP nuclei. In contrast, elderly rats showed increased expression of MT1 and MT2 in CAP stations.

CONCLUSION

These findings suggest that changes in neuronal number and transmission in these nuclei in aging are concomitant with increased melatonin's potential sites of action in the CAP.