Noise alters guinea pig's blood-labyrinth barrier ultrastructure and permeability along with a decrease of cochlear Claudin-5 and Occludin.

BACKGROUND: Noise exposure (NE) is a severe modern health hazard that induces hearing impairment. However, the noise-induced ultrastructural changes of blood-labyrinth barrier (BLB) and the potential involvements of tight junction proteins (TJP) remain inconclusive. We investigated the effects of NE on not only the ultrastructure of cochlea and permeability of BLB but also the expression of TJP within the guinea pig cochlea. RESULTS: Male albino guinea pigs were exposed to white noise for 4 h or 2 consecutive days (115 dB sound pressure level, 6 hours per day) and the hearing impairments and light microscopic change of BLB were evaluated with auditory brainstem responses (ABR) and the cochlear sensory epithelia surface preparation, respectively. The cochlear ultrastructure and BLB permeability after NE 2d were revealed with transmission electron microscope (TEM) and lanthanum nitrate-tracing techniques, respectively. The potential alterations of TJPs Claudin-5 and Occludin were quantified with immunohistochemistry and western blot. NE induced significant hearing impairment and NE 2d contributed to significant outer hair cell (OHC) loss that is most severe in the first row of outer hair cells. Furthermore, the loosen TJ and an obvious leakage of lanthanum nitrate particles beneath the basal lamina were revealed with TEM. Moreover, a dose-dependent decrease of Claudin-5 and Occludin was observed in the cochlea after NE. CONCLUSIONS: All these findings suggest that both decrease of Claudin-5 and Occludin and increased BLB permeability are involved in the pathologic process of noise-induced hearing impairment; however, the causal relationship and underlying mechanisms should be further investigated.

Expression and localization of atrial natriuretic peptide and its receptors in rat spiral ganglion neurons.

Spiral ganglion neurons (SGNs) are the primary auditory neurons in the inner ear, conveying auditory information between sensory hair cells and the central nervous system. Atrial natriuretic peptide (ANP), acting through specific receptors, is a regulatory peptide required for a variety of cardiac and neuronal functions. While the localization of ANP and its receptors (NPR-A and NPR-C) in the inner ear has been widely studied, there is only limited information regarding their localization in cochlear SGNs and their regulatory roles during primary auditory neurotransmission. Here we have investigated the presence of ANP and its receptors in the cochlear spiral ganglion of the postnatal rat using immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. ANP and its receptors are expressed in the cochlear SGNs at both the mRNA and protein level, and co-localize in the cochlear SGNs as shown by immunofluorescence. Our research provides a direct evidence for the presence and synthesis of ANP as well as its receptors in the cochlear SGNs, suggesting a possible role for ANP in modulating the neuronal functions of SGNs via its receptors.