High Blood Glucose Levels Affect Auditory Brainstem Responses after Acoustic Overexposure in Rats

Abstract

Introduction: Diabetes mellitus (DM) is a systemic disease characterized by hyperglycemia and several pathological changes. DM-related hearing dysfunctions are associated with histological changes. Here, we explore hearing function and synaptic changes in the inner hair cells (IHCs) of rats with streptozotocin (STZ)-induced diabetes. Methods: STZ was injected to trigger diabetes. Rats with DM were exposed to narrow-band noise (105 dB SPL) for 2 h, and hearing function was analyzed 1, 3, 7, and 14 days later. Both the hearing threshold and the peak 1 amplitude of the tone auditory brainstem response were assessed. After the last functional test, animals were sacrificed for histological evaluation. Results: We found no changes in the baseline hearing threshold; however, the peak 1 amplitude at the low frequency (4 kHz) was significantly higher in both DM groups than in the control groups. The hearing threshold had not fully recovered at 14 days after diabetic rats were exposed to noise. The peak 1 amplitude at the higher frequencies (16 and 32 kHz) was significantly larger in both DM groups than in the control groups. The histological analysis revealed that the long-term DM group had significantly more synapses in the 16 kHz region than the other groups. Conclusions: We found that high blood glucose levels increased peak 1 amplitudes without changing the hearing threshold. Diabetic rats were less resilient in threshold changes and were less vulnerable to peak 1 amplitude and synaptic damage than control animals.

Active role of glia‐like supporting cells in the organ of Corti: Membrane proteins and their roles in hearing

“…Temporary threshold shifts, due to exposure to intense sound, result in a decrease in hearing sensitivity that recovers over time, whereas in permanent threshold shifts, the decrease in sensitivity does not recover to pre-exposure levels (Ryan et al, 2016). The ABR is permanently reduced when ribbon synapses between IHCs and SGNs are damaged after exposure to continuous noise (Fernandez et al, 2020;Lee et al, 2019;Lee et al, 2020;Lee et al, 2021). Noise briefly upregulates the expression of GLAST and NKAα1, which reduce glutamate or potassium toxicity in the synaptic cleft to prevent cytotoxicity (Ma et al, 2021).…”

Rebokseti̇n’i̇n Di̇yabeti̇k Siçanlarda Bozulmuş Davraniş Parametreleri̇ Üzeri̇ndeki̇ Yararli Etki̇leri̇

“…Bununla birlikte reboksetin'in SSS'de diyabet ile indüklenen moleküler düzeydeki bozuklukları restore etmiş olması da mümkün olabilir. Nitekim reboksetin'in de üyesi olduğu antidepresan ilaçların diyabetik deneklerin beyinlerindeki yetersiz LTP indüksiyonunu, azalan sinaptik protein seviyelerini (sinaptofizin, postsinaptik yoğunluk 95 gibi) ve zayıflayan sinaptik gücü [75,76] iyileştirme potansiyeline sahip oldukları bilinmektedir [73,[77][78][79]. Bu düşünceyi destekler nitlikte olmak üzere; araştırma grubumuz tarafından daha önce yapılan bir çalışmada antidepresan bir ilaç olan agomelatin'in (40 ve 80 mg/kg, 2 hafta) STZ-diyabetik sıçanların öğrenme ve bellek performanslarında kayda değer bir iyileşme sağladığı ve bu hayvanların beyinlerinde hipokampal alt alanlardaki nöron kayıplarını önlediği gösterilmiştir [80].…”