Rajda, Kriti (2021) The role of Cav3.2 channels in noise-induced hearing loss. Research Project 1 (minor thesis), Behavioural and Cognitive Neurosciences.
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Abstract
The prevalence of noise-induced hearing loss (NIHL) has been growing since the onset of the 21st century. The molecular pathology of NIHL is not yet well-known; previous research points to dysregulation of calcium homeostasis in the inner ear being an important cause. In this study, we focus on the role of the Cav3.2 ion channel in cochlear response to noise exposure. Voltage-gated calcium channels (VGCCs) have an α-subunit with ten possible isoforms. In this study, we focus on the Cav3.2 isoform. Earlier studies show that Cav3.2 knockout (KO) mice at five months show elevated auditory thresholds compared to wild type (WT) mice. However, considering their advanced age, absence of this channel may merely accelerate age-related hearing loss. The study examines effects of noise exposure on Cav3.2 KO and heterozygous (HET) mice at six weeks. This was done through auditory brainstem response (ABR) studies on WT, KO and HET mice, in baseline conditions, 24-hour, 7-day and 14-day intervals after noise exposure. At baseline, KO mice had elevated auditory thresholds. After noise exposure, hearing was worsened from the baseline in both WT and KO mice. Inner hair cells and associated synapses of the mice’s cochleae were also counted and no significant differences were seen. The current conclusions of the study are that absence of both copies of the CACNA1H gene impairs hearing and affects the extent to which noise exposure damages it, making KO mice susceptible to hearing impairment.
| Item Type: | Thesis (Research Project 1 (minor thesis)) |
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| Supervisor name: | Persic, D. |
| Degree programme: | Behavioural and Cognitive Neurosciences |
| Thesis type: | Research Project 1 (minor thesis) |
| Language: | English |
| Date Deposited: | 20 Sep 2021 09:59 |
| Last Modified: | 20 Sep 2021 09:59 |
| URI: | https://fse.studenttheses.ub.rug.nl/id/eprint/26079 |
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