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Cochlear Implant Surgery and Electrically-evoked Auditory Brainstem Response Recordings in C57BL/6 Mice
Published on: January 9, 2019
Stimulation by cochlear implant in unilaterally deaf rats reverses the decrease of inhibitory transmission in the
Meritxell Argence1, Isabelle Vassias, Lubin Kerhuel
1Laboratoire de Neurobiologie des Réseaux Sensorimoteurs, Université Paris Descartes - CNRS, Centre Universitaire des Saints-Pères, Paris, France.
The European Journal of Neuroscience
|November 1, 2008
Summary
Electrical stimulation of the deafferented auditory nerve reversed decreased inhibitory neurotransmission in the central nucleus of the inferior colliculus after cochlear injury. This effect was temporary, suggesting a potential tinnitus treatment for unilateral hearing loss.
Area of Science:
- Neuroscience
- Auditory System Research
- Synaptic Plasticity
Background:
- Unilateral cochlear injury alters synaptic transmission in auditory nuclei.
- Limited data exists on electrical stimulation's effect on inhibitory neurotransmission post-cochlear injury.
Purpose of the Study:
- Investigate the impact of chronic electrical stimulation of the deafferented auditory nerve on inhibitory neurotransmission markers in the central nucleus of the inferior colliculus (CIC).
- Examine the expression of the alpha1 subunit of the glycinergic receptor (GlyRalpha1) and glutamic acid decarboxylase (GAD)67.
Main Methods:
- Unilateral cochlear injury induced via neomycin sulfate in adult rats.
- Chronic electrical stimulation of the deafferented auditory nerve for varying durations (4, 8, 22 h daily) over 5 days.
- Quantification of GlyRalpha1 and GAD67 mRNA and protein in the CIC using in situ hybridization and immunohistofluorescence.
Main Results:
- Unilateral cochlear injury significantly decreased GlyRalpha1 and GAD67 expression in the contralateral CIC.
- Chronic electrical stimulation of the deafferented auditory nerve reversed these down-regulations.
- The recovery of expression levels persisted for less than 5 days after stimulation cessation.
Conclusions:
- Down-regulation of GlyRalpha1 and GAD67 may contribute to increased CIC excitability and tinnitus in unilateral deafness.
- Electrical stimulation of the deafferented auditory nerve shows potential as a therapeutic approach for tinnitus in patients with unilateral hearing loss.

