Monaural conductive hearing loss alters the expression of the GluA3 AMPA and glycine receptor α1 subunits in bushy and fusiform cells of the cochlear nucleus.
Summary of "Monaural conductive hearing loss alters the expression of the GluA3 AMPA and glycine receptor α1 subunits in bushy and fusiform cells of the cochlear nucleus."
The impact of conductive hearing loss (CHL), the second most common form of hearing loss, on neuronal plasticity in the central auditory pathway is unknown. After short-term (1 day) monaural earplugging, the GluA3 subunits of the AMPA receptor (AMPAR) are upregulated at auditory nerve synapses on the projection neurons of the cochlear nucleus; glycine receptor α1 (GlyRα1) subunits are downregulated at inhibitory synapses in the same neuronal population. These data suggest that CHL affects receptor trafficking at synapses. We examined the impact of 7 days of CHL on the general expression of excitatory and inhibitory receptors by quantitative biochemistry and immunohistochemistry, using specific antibodies to detect AMPAR subunits (GluA1, GluA2, GluA2/3, and GluA4), GlyRα1, and the GABA(A) receptor subunits β2/3. Following monaural earplugging and an elevation of the hearing threshold by approximately 35 dB, the immunolabeling of the antibody for the GluA2/3 subunits but not the GluA2 subunit increased on bushy cells (BCs) and fusiform cells (FCs) of the ipsilateral ventral and dorsal cochlear nuclei. These same cell types showed a downregulation of the GlyRα1 subunit. Similar results were observed in the contralateral nuclei. The expression levels of GABA(A) β2/3 were unchanged. These findings suggest that, following longer periods of monaural conductive hearing loss, the synthesis and subsequent composition of specific glutamate and glycine receptors in projection neurons and their synapses are altered; these changes may contribute to abnormal auditory processing.
Affiliation
Department of Otolaryngology, University of Pittsburgh, 3501 5th Avenue BST3 10015, Pittsburgh, PA 15261, USA.
Journal Details
This article was published in the following journal.
Name: Neuroscience
ISSN: 1873-7544
Pages: 438-51
Links
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22044924
- DOI: http://dx.doi.org/10.1016/j.neuroscience.2011.10.021
Medical and Biotech [MESH] Definitions
Hearing Loss, Mixed Conductive-sensorineural
Hearing loss due to damage or impairment of both the conductive elements (HEARING LOSS, CONDUCTIVE) and the sensorineural elements (HEARING LOSS, SENSORINEURAL) of the ear.
Glomus Tympanicum Tumor
A rare PARAGANGLIOMA involving the GLOMUS TYMPANICUM, a collection of chemoreceptor tissue adjacent to the TYMPANIC CAVITY. It can cause TINNITUS and conductive hearing loss (HEARING LOSS, CONDUCTIVE).
Hearing Loss, Conductive
Hearing loss due to interference with the mechanical reception or amplification of sound to the COCHLEA. The interference is in the outer or middle ear involving the EAR CANAL; TYMPANIC MEMBRANE; or EAR OSSICLES.
Hearing Loss, Noise-induced
Hearing loss due to exposure to explosive loud noise or chronic exposure to sound level greater than 85 dB. The hearing loss is often in the frequency range 4000-6000 hertz.
Hearing Loss, Central
Hearing loss due to disease of the AUDITORY PATHWAYS (in the CENTRAL NERVOUS SYSTEM) which originate in the COCHLEAR NUCLEI of the PONS and then ascend bilaterally to the MIDBRAIN, the THALAMUS, and then the AUDITORY CORTEX in the TEMPORAL LOBE. Bilateral lesions of the auditory pathways are usually required to cause central hearing loss. Cortical deafness refers to loss of hearing due to bilateral auditory cortex lesions. Unilateral BRAIN STEM lesions involving the cochlear nuclei may result in unilateral hearing loss.
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