RGD Reference Report - Tracking the expression of excitatory and inhibitory neurotransmission-related proteins and neuroplasticity markers after noise induced hearing loss. - Rat Genome Database

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Tracking the expression of excitatory and inhibitory neurotransmission-related proteins and neuroplasticity markers after noise induced hearing loss.

Authors: Browne, Cherylea J  Morley, John W  Parsons, Carl H 
Citation: Browne CJ, etal., PLoS One. 2012;7(3):e33272. doi: 10.1371/journal.pone.0033272. Epub 2012 Mar 12.
RGD ID: 401940127
Pubmed: PMID:22428005   (View Abstract at PubMed)
PMCID: PMC3299769   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.pone.0033272   (Journal Full-text)

Excessive exposure to loud noise can damage the cochlea and create a hearing loss. These pathologies coincide with a range of CNS changes including reorganisation of frequency representation, alterations in the pattern of spontaneous activity and changed expression of excitatory and inhibitory neurotransmitters. Moreover, damage to the cochlea is often accompanied by acoustic disorders such as hyperacusis and tinnitus, suggesting that one or more of these neuronal changes may be involved in these disorders, although the mechanisms remain unknown. We tested the hypothesis that excessive noise exposure increases expression of markers of excitation and plasticity, and decreases expression of inhibitory markers over a 32-day recovery period. Adult rats (n = 25) were monaurally exposed to a loud noise (16 kHz, 1/10(th) octave band pass (115 dB SPL)) for 1-hour, or left as non-exposed controls (n = 5). Animals were euthanased at either 0, 4, 8, 16 or 32 days following acoustic trauma. We used Western Blots to quantify protein levels of GABA(A) receptor subunit α1 (GABA(A)α1), Glutamic-Acid Decarboxylase-67 (GAD-67), N-Methyl-D-Aspartate receptor subunit 2A (NR2A), Calbindin (Calb1) and Growth Associated Protein 43 (GAP-43) in the Auditory Cortex (AC), Inferior Colliculus (IC) and Dorsal Cochlear Nucleus (DCN). Compared to sham-exposed controls, noise-exposed animals had significantly (p<0.05): lower levels of GABA(A)α1 in the contralateral AC at day-16 and day-32, lower levels of GAD-67 in the ipsilateral DCN at day-4, lower levels of Calb1 in the ipsilateral DCN at day-0, lower levels of GABA(A)α1 in the ipsilateral AC at day-4 and day-32. GAP-43 was reduced in the ipsilateral AC for the duration of the experiment. These complex fluctuations in protein expression suggests that for at least a month following acoustic trauma the auditory system is adapting to a new pattern of sensory input.




Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Calb1Ratresponse to auditory stimulus  IEP  RGD 
Gabra1Ratresponse to auditory stimulus  IEP  RGD 
Gad1Ratresponse to auditory stimulus  IEP  RGD 
Gap43Ratresponse to auditory stimulus  IEP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Calb1  (calbindin 1)
Gabra1  (gamma-aminobutyric acid type A receptor subunit alpha 1)
Gad1  (glutamate decarboxylase 1)
Gap43  (growth associated protein 43)

Genes (Mus musculus)
Calb1  (calbindin 1)
Gabra1  (gamma-aminobutyric acid type A receptor subunit alpha 1)
Gad1  (glutamate decarboxylase 1)
Gap43  (growth associated protein 43)

Genes (Homo sapiens)
CALB1  (calbindin 1)
GABRA1  (gamma-aminobutyric acid type A receptor subunit alpha1)
GAD1  (glutamate decarboxylase 1)
GAP43  (growth associated protein 43)


Additional Information