Abstract
We evaluated the role of iron deficiency (ID) without anemia on hearing function and cochlear pathophysiology of young rats before and after noise exposure. We used rats at developmental stages as an animal model to induce ID without anemia by dietary iron restriction. We have established this dietary restriction model in the rat that should enable us to study the effects of iron deficiency in the absence of severe anemia on hearing and ribbon synapses. Hearing function was measured on Postnatal Day (PND) 21 after induction of ID using auditory brainstem response (ABR). Then, the young rats were exposed to loud noise on PND 21. After noise exposure, hearing function was again measured. We observed the morphology of ribbon synapses, hair cells and spiral ganglion cells (SGCs), and assessed the expression of myosin VIIa, vesicular glutamate transporter 3 and prestin in the cochlea. ID without anemia did not elevate ABR threshold shifts, but reduced ABR wave I peak amplitude of young rats. At 70, 80, and 90 dB SPL, amplitudes of wave I (3.11 ± 0.96 µV, 3.52 ± 1.31 µV, and 4.37 ± 1.08 µV, respectively) in pups from the ID group were decreased compared to the control (5.92 ± 1.67 µV, 6.53 ± 1.70 µV, and 6.90 ± 1.76 µV, respectively) (p < 0.05). Moreover, ID without anemia did not impair the morphology hair cells and SGCs, but decreased the number of ribbon synapses. Before noise exposure, the mean number of ribbon synapses per inner hair cell (IHC) was significantly lower in the ID group (8.44 ± 1.21) compared to that seen in the control (13.08 ± 1.36) (p < 0.05). In addition, the numbers of ribbon synapses per IHC of young rats in the control (ID group) were 6.61 ± 1.59, 3.07 ± 0.83, 5.85 ± 1.63 and 12.25 ± 1.97 (3.75 ± 1.45, 2.03 ± 1.08, 3.81 ± 1.70 and 4.01 ± 1.65) at 1, 4, 7 and 14 days after noise exposure, respectively. Moreover, ABR thresholds at 4 and 8 kHz in young rats from the ID group were significantly elevated at 7 and 14 days after noise exposure compared to control (p < 0.05). The average number of young rat SGCs from the ID group were significantly decreased in the basal turn of the cochlea compared to the control (p < 0.05). Therefore, ID without anemia delayed the recovery from noise-induced hearing loss and ribbon synapses damage, increased SGCs loss, and upregulated prestin after noise exposure. Thus, the cochleae in rat pups with ID without anemia were potentially susceptible to loud noise exposure, and this deficit may be attributed to the reduction of ribbon synapses and SGCs.
Highlights
Iron deficiency (ID), the most common form of micronutrient deficiency, is the primary cause of anemia, which affects more than two billion people, especially children and pregnant women [1,2,3,4]
We observed no differences in iron deficiency (ID)-related auditory brainstem response (ABR) threshold changes and between the control and ID rats before noise significant differences in ID‐related ABR threshold changes and between the control and ID rats exposure, we only observed a significant difference in the amplitudes of wave I peak between two before noise exposure, we only observed a significant difference in the amplitudes of wave I peak groups
We showed that recovery from and ribbon synapses injury was significantly impaired in this ID model in the absence of anemia, noise‐induced hearing and ribbon synapses injury was significantly impaired in this ID model in the accompanied by the increase of spiral ganglion cells (SGCs) loss and upregulation of prestin in the cochleae
Summary
Iron deficiency (ID), the most common form of micronutrient deficiency, is the primary cause of anemia, which affects more than two billion people, especially children and pregnant women [1,2,3,4]. Myosin VIIa contributes to regulate vesicle cycling of cochlear hair cells, and VGLUT3 contributes to the loading of glutamate into the synaptic vesicles [19,20]. A recent study showed that mild maternal IDA downregulated VGLUT3 and myosin VIIa, and upregulated prestin in the cochleae of young guinea pigs [22]. We attempted to ascertain whether ID without anemia could primarily affect the inner ear of offspring by increasing its sensitivity to noise exposure. This hypothesis was tested by comparing the sensitivity to noise-induced hearing loss in normal rats versus ID rats in the absence of anemia
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