RGD Reference Report - Long-lasting changes in the cochlear K recycling structures after acute energy failure. - Rat Genome Database

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Long-lasting changes in the cochlear K recycling structures after acute energy failure.

Authors: Takiguchi, Y  Sun, GW  Ogawa, K  Matsunaga, T 
Citation: Takiguchi Y, etal., Neurosci Res. 2013 Jul 1. pii: S0168-0102(13)00159-4. doi: 10.1016/j.neures.2013.06.003.
RGD ID: 7349365
Pubmed: PMID:23827367   (View Abstract at PubMed)
DOI: DOI:10.1016/j.neures.2013.06.003   (Journal Full-text)

Fibrocytes in the cochlear lateral wall and spiral limbus play an important role in transporting K+ and have the capacity of self-renewal. We showed that acute energy failure in the rat cochlea induced by local administration of the mitochondrial toxin 3-nitropropionic acid (3NP) caused hearing loss in a concentration-dependent manner, mainly due to degeneration of cochlear fibrocytes. We produced long-lasting profound cochlear damage in this model by modifying the 3NP administration protocol and observed morphological changes at 16 weeks after the administration. In the spiral ligament, severe degeneration of fibrocytes was observed in the basal turn, and the levels of the Na,K-ATPase alpha and beta1 subunits and of NKCC1 were decreased in these cells, whereas connexin 26 (Cx26) level increased in the type 1 fibrocytes adjacent to the stria vascularis. In the stria vascularis, levels of Kir4.1 and L-PGDS decreased. In the spiral limbus, severe degeneration of fibrocytes was observed in the middle and basal turns, but NKCC1 and Cx26 were still found in the center of the limbus in the middle turn. These results indicate long-lasting changes in the cochlear lateral wall and spiral limbus, which may compensate for damaged K+ recycling and protect cells from ATP shortage.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
sensorineural hearing loss  ISOAtp1a1 (Rattus norvegicus)7349365; 7349365protein:decreased expression:cochlea:RGD 
sensorineural hearing loss  ISOAtp1b1 (Rattus norvegicus)7349365; 7349365protein:decreased expression:cochlea:RGD 
sensorineural hearing loss  IEP 7349365; 7349365; 7349365; 7349365; 7349365protein:decreased expression:cochlea:RGD 
sensorineural hearing loss  ISOGjb2 (Rattus norvegicus)7349365; 7349365protein:increased expression:cochlea:RGD 
sensorineural hearing loss  IEP 7349365protein:increased expression:cochlea:RGD 
sensorineural hearing loss  ISOKcnj10 (Rattus norvegicus)7349365; 7349365protein:decreased expression:cochlea:RGD 
sensorineural hearing loss  ISOPtgds (Rattus norvegicus)7349365; 7349365protein:decreased expression:cochlea:RGD 
sensorineural hearing loss  ISOSlc12a2 (Rattus norvegicus)7349365; 7349365protein:decreased expression:cochlea:RGD 

Objects Annotated

Genes (Rattus norvegicus)
Atp1a1  (ATPase Na+/K+ transporting subunit alpha 1)
Atp1b1  (ATPase Na+/K+ transporting subunit beta 1)
Gjb2  (gap junction protein, beta 2)
Kcnj10  (potassium inwardly-rectifying channel, subfamily J, member 10)
Ptgds  (prostaglandin D2 synthase)
Slc12a2  (solute carrier family 12 member 2)

Genes (Mus musculus)
Atp1a1  (ATPase, Na+/K+ transporting, alpha 1 polypeptide)
Atp1b1  (ATPase, Na+/K+ transporting, beta 1 polypeptide)
Gjb2  (gap junction protein, beta 2)
Kcnj10  (potassium inwardly-rectifying channel, subfamily J, member 10)
Ptgds  (prostaglandin D2 synthase (brain))
Slc12a2  (solute carrier family 12, member 2)

Genes (Homo sapiens)
ATP1A1  (ATPase Na+/K+ transporting subunit alpha 1)
ATP1B1  (ATPase Na+/K+ transporting subunit beta 1)
GJB2  (gap junction protein beta 2)
KCNJ10  (potassium inwardly rectifying channel subfamily J member 10)
PTGDS  (prostaglandin D2 synthase)
SLC12A2  (solute carrier family 12 member 2)


Additional Information