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Data Acquisition and Analysis In Brainstem Evoked Response Audiometry In Mice
Published on: May 10, 2019
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Elevated auditory brainstem response thresholds in mice with Connexin36 gene ablation.
Brian W Blakley1, Carlos E A Garcia, Suzete R da Sliva
1Department of Otolaryngology, University of Manitoba , Winnipeg , Canada.
Acta Oto-Laryngologica
|April 21, 2015
Summary
Connexin36 (Cx36) forms electrical synapses crucial for normal auditory brainstem response thresholds in mice. Loss of Cx36 impairs brainstem auditory function, highlighting its role in hearing.
Area of Science:
- Neuroscience
- Auditory System Research
- Molecular Biology
Background:
- Electrical synaptic transmission via gap junctions is understudied in the auditory system.
- Connexin36 (Cx36) is the primary protein forming neuronal gap junctions in the mammalian brain.
Purpose of the Study:
- To investigate the role of Cx36 in murine hearing.
- To evaluate the impact of Cx36 knockout on auditory function.
Main Methods:
- Auditory brainstem response (ABR) thresholds were measured in wild-type and Cx36 knockout mice.
- Distortion product otoacoustic emissions (DPOAEs) were used to assess cochlear function.
Main Results:
- Cochlear function was similar between Cx36 knockout and wild-type mice, as indicated by DPOAEs.
- ABR thresholds were significantly elevated in Cx36 knockout mice, indicating impaired auditory brainstem function.
- Findings suggest Cx36-containing gap junctions are vital for brainstem auditory processing, not cochlear function.
Conclusions:
- Cx36 expression and its electrical synapses are essential for normal auditory brainstem response thresholds.
- These findings are significant for understanding human auditory pathologies.
- Cx36 plays a critical role in auditory sound processing at the brainstem level.
Keywords:
distortion product otoacoustic emissionselectrical synapsesgap junctionshearing deficienciesneurons
