Lundt, Andreas, Seidel, Robin, Soos, Julien, Henseler, Christina, Mueller, Ralf, Bakki, Maheshwar, Arshaad, Muhammad Imran, Ehninger, Dan, Hescheler, Juergen, Sachinidis, Agapios, Broich, Karl, Wormuth, Carola, Papazoglou, Anna and Weiergraeber, Marco (2019). Ca(v)3.2 T-Type Calcium Channels Are Physiologically Mandatory for the Auditory System. Neuroscience, 409. S. 81 - 101. OXFORD: PERGAMON-ELSEVIER SCIENCE LTD. ISSN 1873-7544

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Abstract

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, Ca(v)3.2 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 Ca(v)3.2(+/-) and Ca(v)3.2(-/-) 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 Ca(v)3.2 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 Ca(v)3.2 VGCCs in the spatiotemporal organization of auditory processing in young adult mice and suggest potential pharmacological targets for interventions in the future. (C) 2019 The Author(s). Published by Elsevier Ltd on behalf of IBRO.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Lundt, AndreasUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Seidel, RobinUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Soos, JulienUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Henseler, ChristinaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Mueller, RalfUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Bakki, MaheshwarUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Arshaad, Muhammad ImranUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ehninger, DanUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Hescheler, JuergenUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Sachinidis, AgapiosUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Broich, KarlUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Wormuth, CarolaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Papazoglou, AnnaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Weiergraeber, MarcoUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-137756
DOI: 10.1016/j.neuroscience.2019.04.024
Journal or Publication Title: Neuroscience
Volume: 409
Page Range: S. 81 - 101
Date: 2019
Publisher: PERGAMON-ELSEVIER SCIENCE LTD
Place of Publication: OXFORD
ISSN: 1873-7544
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
SPIRAL GANGLION NEURONS; SENSORINEURAL HEARING-LOSS; CA(V)1.3 CA2+ CHANNELS; BRAIN-STEM RESPONSES; CARDIOVASCULAR-DISEASE; THERAPEUTIC FUNCTIONS; MOUSE MODELS; MICE; DYSFUNCTION; EXPRESSIONMultiple languages
NeurosciencesMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/13775

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