RGD Reference Report - Effects of salicylate on the inflammatory genes expression and synaptic ultrastructure in the cochlear nucleus of rats. - Rat Genome Database

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Effects of salicylate on the inflammatory genes expression and synaptic ultrastructure in the cochlear nucleus of rats.

Authors: Hu, Shou-Sen  Mei, Ling  Chen, Jian-Yong  Huang, Zhi-Wu  Wu, Hao 
Citation: Hu SS, etal., Inflammation. 2014 Apr;37(2):365-73. doi: 10.1007/s10753-013-9748-2.
RGD ID: 401940125
Pubmed: PMID:24092407   (View Abstract at PubMed)
DOI: DOI:10.1007/s10753-013-9748-2   (Journal Full-text)

Aspirin (salicylate), as a common drug that is frequently used for long-term treatment in a clinical setting, has the potential to cause reversible tinnitus. However, few reports have examined the inflammatory cytokines expression and alteration of synaptic ultrastructure in the cochlear nucleus (CN) in a rat model of tinnitus. The tinnitus-like behavior of rats were detected by the gap prepulse inhibition of acoustic startle (GPIAS) paradigm. We investigated the expression levels of the tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), N-methyl D-aspartate receptor subunit 2A (NR2A) mRNA and protein in the CN and compared synapses ultrastructure in the CN of tinnitus rats with normal ones. GPIAS showed that rats with long-term administration of salicylate were experiencing tinnitus, and the mRNA and protein expression levels of TNF-α and NR2A were up-regulated in chronic treatment groups, and they returned to baseline 14 days after cessation of treatment. Furthermore, compared to normal rats, repetitive salicylate-treated rats showed a greater number of presynaptic vesicles, thicker and longer postsynaptic densities, increased synaptic interface curvature. These data revealed that chronic salicylate administration markedly, but reversibly, induces tinnitus possibly via augmentation of the expression of TNF-α and NR2A and cause changes in synaptic ultrastructure in the CN. Long-term administration of salicylate causes neural plasticity changes at the CN level.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
GRIN2AHumanTinnitus  ISOGrin2a (Rattus norvegicus)mRNA and protein:increased expression:Cochlear NucleusRGD 
Grin2aRatTinnitus  IEP mRNA and protein:increased expression:Cochlear NucleusRGD 
Grin2aMouseTinnitus  ISOGrin2a (Rattus norvegicus)mRNA and protein:increased expression:Cochlear NucleusRGD 
TNFHumanTinnitus  ISOTnf (Rattus norvegicus)mRNA and protein:increased expression:Cochlear NucleusRGD 
TnfRatTinnitus  IEP mRNA and protein:increased expression:Cochlear NucleusRGD 
TnfMouseTinnitus  ISOTnf (Rattus norvegicus)mRNA and protein:increased expression:Cochlear NucleusRGD 

Objects Annotated

Genes (Rattus norvegicus)
Grin2a  (glutamate ionotropic receptor NMDA type subunit 2A)
Tnf  (tumor necrosis factor)

Genes (Mus musculus)
Grin2a  (glutamate receptor, ionotropic, NMDA2A (epsilon 1))
Tnf  (tumor necrosis factor)

Genes (Homo sapiens)
GRIN2A  (glutamate ionotropic receptor NMDA type subunit 2A)
TNF  (tumor necrosis factor)


Additional Information