RGD Reference Report - Impact of sound exposure and aging on brain-derived neurotrophic factor and tyrosine kinase B receptors levels in dorsal cochlear nucleus 80 days following sound exposure. - Rat Genome Database

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Impact of sound exposure and aging on brain-derived neurotrophic factor and tyrosine kinase B receptors levels in dorsal cochlear nucleus 80 days following sound exposure.

Authors: Wang, H  Brozoski, TJ  Ling, L  Hughes, LF  Caspary, DM 
Citation: Wang H, etal., Neuroscience. 2011 Jan 13;172:453-9. Epub 2010 Oct 27.
RGD ID: 5684781
Pubmed: PMID:21034795   (View Abstract at PubMed)
PMCID: PMC3057525   (View Article at PubMed Central)
DOI: DOI:10.1016/j.neuroscience.2010.10.056   (Journal Full-text)

Recent studies suggested that acute sound exposure resulting in a temporary threshold shift in young adult animals within a series of maladaptive plasticity changes in central auditory structures. Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, is involved in post-trauma peripheral hair cell and spiral ganglion cell survival and has been shown to modulate synaptic strength in cochlear nucleus following sound exposure. The present study evaluated levels of BDNF and its receptor (tyrosine kinase B, [TrkB]) in the dorsal cochlear nucleus (DCN) following a unilateral moderate sound exposure in young (7-8 months) and aged (28-29 months) Fischer Brown Norway (FBN) rats. Eighty days post-exposure, auditory brainstem response (ABR) thresholds for young exposed rats approached control values while aged exposed rats showed residual permanent threshold shifts (PTS) relative to aged controls. BDNF protein levels were significantly up-regulated by 9% in young exposed fusiform cells ipsilateral to the exposure. BDNF levels in aged sound-exposed fusiform cells increased 31% ipsilateral to the exposure. Protein levels of the BDNF receptor, TrkB, were also significantly increased in aged but not in young sound-exposed DCN fusiform cells. The present findings suggest a relationship between the up-regulation of BDNF/TrkB and the increase in spontaneous and driven activity previously observed for aged and sound-exposed fusiform cells. This might be due to a selective maladaptive compensatory down-regulation of glycinergic inhibition in DCN fusiform cells.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
BdnfRatresponse to auditory stimulus  IEP  RGD 
Ntrk2Ratresponse to auditory stimulus  IEP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Bdnf  (brain-derived neurotrophic factor)
Ntrk2  (neurotrophic receptor tyrosine kinase 2)


Additional Information