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Home › Dataset Library › Temporal profiling of gene expression in cochleae of wild type and alpha9 null mice

Dataset: Temporal profiling of gene expression in cochleae of wild type and alpha9 null mice

Efferent inhibition of cochlear outer hair cells is mediated by nicotinic cholinergic receptors containing alpha9 (a9) and alpha10...

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Efferent inhibition of cochlear outer hair cells is mediated by nicotinic cholinergic receptors containing alpha9 (a9) and alpha10 subunits. Mice lacking a9 nicotinic subunits fail to exhibit classic olivocochlear responses and are characterized by abnormal synaptic morphology at the base of outer hair cells. To detail molecular changes induced upon the loss of a9 subunit, we sampled cochlear RNA from wild type and a9 null mice at postnatal (P) days spanning periods of synapse formation and maturation (P3, P7, P13 and P60). Our findings point to a delay in cochlear maturation starting at the onset of hearing (P13), as well as an up-regulation of various GABA receptor subunits in adult mice lacking the a9 nicotinic subunit. Cochleae were removed at postnatal ages P3, P7, P13 and P60. Cochlear tissues from 3-5 mice were pooled per replicate; biological triplicates were performed for each age and genotype.

Species:
mouse

Samples:
24

Source:
E-GEOD-18567

PubMed:
20140217

Updated:
Dec.12, 2014

Registered:
Nov.11, 2014


Factors: (via ArrayExpress)
Sample AGE GENOTYPE
GSM462007 P3 wild_type
GSM462007 P3 wild_type
GSM462007 P3 wild_type
GSM462010 P3 a9 knockout
GSM462010 P3 a9 knockout
GSM462010 P3 a9 knockout
GSM462013 P7 wild_type
GSM462013 P7 wild_type
GSM462013 P7 wild_type
GSM462016 P7 a9 knockout
GSM462016 P7 a9 knockout
GSM462016 P7 a9 knockout
GSM462019 P13 wild_type
GSM462019 P13 wild_type
GSM462019 P13 wild_type
GSM462022 P13 a9 knockout
GSM462022 P13 a9 knockout
GSM462022 P13 a9 knockout
GSM462025 P60 wild_type
GSM462025 P60 wild_type
GSM462025 P60 wild_type
GSM462028 P60 a9 knockout
GSM462028 P60 a9 knockout
GSM462028 P60 a9 knockout

Tags

  • hair
  • point
  • synapse

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