Transcriptomics

Dataset Information

4

Transcription profiling of mouse dorsal root ganglia after diphtheria-toxin deletion of the Nav1.8-expressing cells using the cre/loxP system


ABSTRACT: Comparison of transcript levels after diphtheria-toxin deletion of the Nav1.8-expressing cells using the cre/loxP system.
Pain requires input from nociceptors which are specialised peripheral sensory neurons in dorsal root ganglia (DRG). To explore the nociceptor-specific mRNA profiles, we used microarray analysis to examine the altered repertoire of genes expressed in DRG from mice depleted of Nav1.8-expressing neurons which are mainly nociceptors. To generate the animal, a Nav1.8 knock-in Cre-expressing mouse (Nav1.8-Cre) was used to excise a floxed stop upstream of globally expressed diphtheria toxin A-subunit gene (ROSA26-eGFP-DTA). By crossing heterozygous Cre mice with homozygous toxin-expressing floxed mice, experimental toxin-expressing (DTA) mice, in which DTA expressing nociceptors had been deleted, were generated. 6 DTA mice and 6 litter mate controls were used for microarray analysis. 3 Affymetrix Mouse Genome 430 2.0 Array chips were employed for analysis of the gene transcripts of each conditions.

INSTRUMENT(S): 418 [Affymetrix]

ORGANISM(S): Mus musculus  

SUBMITTER: Jing Zhao  

PROVIDER: E-MEXP-1622 | ArrayExpress | 2008-08-02

REPOSITORIES: ArrayExpress

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Publications

The cell and molecular basis of mechanical, cold, and inflammatory pain.

Abrahamsen Bjarke B   Zhao Jing J   Asante Curtis O CO   Cendan Cruz Miguel CM   Marsh Steve S   Martinez-Barbera Juan Pedro JP   Nassar Mohammed A MA   Dickenson Anthony H AH   Wood John N JN  

Science (New York, N.Y.) 20080801 5889


Peripheral pain pathways are activated by a range of stimuli. We used diphtheria toxin to kill all mouse postmitotic sensory neurons expressing the sodium channel Nav1.8. Mice showed normal motor activity and low-threshold mechanical and acute noxious heat responses but did not respond to noxious mechanical pressure or cold. They also showed a loss of enhanced pain responses and spontaneous pain behavior upon treatment with inflammatory insults. In contrast, nerve injury led to heightened pain s  ...[more]

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