Cav3.2 T-Type Calcium Channels Are Physiologically Mandatory for the Auditory System
| Autor: | Anna Papazoglou, Maheshwar Bakki, Christina Henseler, Ralf Müller, Muhammad Imran Arshaad, Robin Seidel, Julien Soos, Jürgen Hescheler, Marco Weiergräber, Carola Wormuth, Agapios Sachinidis, Andreas Lundt, Dan Ehninger, Karl Broich |
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| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Auditory perception Hearing loss genetics [Hearing Loss] metabolism [Calcium Channels T-Type] Biology physiology [Hearing] 03 medical and health sciences Mice Calcium Channels T-Type 0302 clinical medicine metabolism [Hearing Loss] genetics [Calcium Channels T-Type] otorhinolaryngologic diseases medicine Auditory system Animals ddc:610 Cochlea Mice Knockout General Neuroscience T-type calcium channel medicine.disease Cacna1h protein mouse physiology [Auditory Threshold] 030104 developmental biology Auditory brainstem response medicine.anatomical_structure Sensorineural hearing loss metabolism [Cochlea] medicine.symptom Neuroscience 030217 neurology & neurosurgery Noise-induced hearing loss |
| Zdroj: | Neuroscience 409, 81-100 (2019). doi:10.1016/j.neuroscience.2019.04.024 |
| DOI: | 10.1016/j.neuroscience.2019.04.024 |
| Popis: | Voltage-gated Ca2+ channels (VGCCs) play key roles in auditory perception and information processing within the inner ear and brainstem. Pharmacological inhibition of low voltage-activated (LVA) T-type Ca2+ channels is related to both age- and noise induced hearing loss in experimental animals and may represent a promising approach to the treatment of auditory impairment of various etiologies. Within the LVA Ca2+ channel subgroup, Cav3.2 is the most prominently expressed T-type channel entity in the cochlea and auditory brainstem. Thus, we performed a complete gender specific click and tone burst based auditory brainstem response (ABR) analysis of Cav3.2+/- and Cav3.2-/- mice, including i.a. temporal progression in hearing loss, amplitude growth function and wave latency analysis as well as a cochlear qPCR based evaluation of other VGCCs transcripts. Our results, based on a self-programmed automated wavelet approach, demonstrate that both heterozygous and Cav3.2 null mutant mice exhibit age-dependent increases in hearing thresholds at 5 months of age. In addition, complex alterations in WI-IV amplitudes and latencies were detected that were not attributable to alterations in the expression of other VGCCs in the auditory tract. Our results clearly demonstrate the important physiological role of Cav3.2 VGCCs in the spatiotemporal organization of auditory processing in young adult mice and suggest potential pharmacological targets for interventions in the future. |
| Databáze: | OpenAIRE |
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