The purinergic receptors 2X3 on spiral ganglion neurons enhance the medial olivocochlear reflex in mice after long-term moderate noise exposure

by Selleckchem | Oct 07 2023

Our purpose was to study the expression of purinergic receptors 2X2 (P2X2) and purinergic receptors 2X3 (P2X3) in spiral ganglion neurons (SGNs), the afferent nerves of medial olivocochlear (MOC) reflex, after long-term moderate noise exposure, and its relationship with the enhancement of MOC reflex. Mice were exposed a moderate broadband noise for 4 weeks consecutively. Then mouse hearing functions, including threshold auditory brainstem responses, distortion-product otoacoustic emissions, and MOC reflex, were evaluated and the expression of P2X2 and P2X3 on SGNs were assessed by cochlear immunofluorescence. AF-353 was injected before each noise exposure. Four weeks later, mice were also tested for hearing functions and expression of P2X2 and P2X3 on SGNs. The long-term moderate noise strengthened MOC reflex, and AF-353 reduced it in mice and P2X3 expression on SGNs increased after long-term moderate noise exposure, and AF-353 can downregulate it. The P2X3 on SGNs of mice increased after long-term moderate noise exposure, and the upregulation of it mediated the enhancement of MOC reflex.

Comments:

Your study aimed to investigate the expression of purinergic receptors 2X2 (P2X2) and purinergic receptors 2X3 (P2X3) in spiral ganglion neurons (SGNs) after long-term moderate noise exposure, and its relationship with the enhancement of the medial olivocochlear (MOC) reflex. The MOC reflex refers to the feedback mechanism in the auditory system that involves the efferent nerves originating from the medial olivocochlear bundle.

In your experiment, mice were exposed to moderate broadband noise continuously for 4 weeks. To assess the effects of the noise exposure and the purinergic receptors, various hearing function tests were conducted, including threshold auditory brainstem responses and distortion-product otoacoustic emissions. The MOC reflex was also evaluated. Additionally, the expression of P2X2 and P2X3 on SGNs was examined using cochlear immunofluorescence.

During the noise exposure period, AF-353, a specific antagonist for P2X3 receptors, was injected before each noise exposure. After the 4-week exposure period, mice underwent further hearing function tests, and the expression of P2X2 and P2X3 on SGNs was reassessed.

The results of your study indicated that long-term moderate noise exposure led to a strengthening of the MOC reflex in mice. However, the administration of AF-353 reduced the enhancement of the MOC reflex. This suggests that P2X3 receptors may play a role in mediating the increased MOC reflex activity.

Furthermore, the expression of P2X3 receptors on SGNs increased after the long-term moderate noise exposure. The upregulation of P2X3 receptors on SGNs is likely associated with the enhanced MOC reflex. Importantly, AF-353 was shown to downregulate the expression of P2X3 receptors on SGNs.

In summary, your study provides evidence that long-term moderate noise exposure can strengthen the MOC reflex in mice. This enhancement appears to be mediated by the upregulation of P2X3 receptors on SGNs. The administration of AF-353, which reduces P2X3 receptor activity, attenuates the strengthening of the MOC reflex. These findings suggest a potential mechanism underlying the modulation of the MOC reflex through purinergic signaling pathways involving P2X3 receptors in SGNs.