B6.129X1-Htr3a^tm1Jul/J

Stock number: 005251
Product name: 5-HT₃R-A KO
Research areas: Neurobiology Research, Sensorineural Research

Description

These Htr3a knock-out mice exhibit an impaired response to persistent pain caused by inflammatory tissue injury.

Detailed description

Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of the dorsal root ganglia. Quantitative autoradiography ligand binding assays of solitary tract nucleus, area postrema and trigenimal nucleus caudalis and electrophysiological tests of isolated nociceptor neurons do not detect functional receptor activity. Mutant mice have an impaired response to persistent pain caused by inflammatory tissue injury. This mutant mouse strain may be useful in studies of nociceptive processing, pain response behavior, and peripheral neurogenic inflammation.

Development

A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exons 7 and 8. The construct was electroporated into 129X1/SvJ derived JM1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to C57BL/6 mice, and then backcrossed to the same for 5 generations (April 2005).

Allele

Symbol: Htr3a^tm1Jul
Name: targeted mutation 1, David Julius
MGI accession ID: MGI:3055155
Generation method: Targeted
Attributes: Null/Knockout
Synonyms: Htr3a^tm1Bbm; 5-HT3R-A^-
Marker symbol: Htr3a
Marker name: 5-hydroxytryptamine (serotonin) receptor 3A
Chromosome: 9
Strain of origin: 129X1/SvJ
Molecular note: A PGK-neomycin cassette was inserted in place of exons 7 and 8, which encode the first three putative transmembrane domains of the channel protein. Northern blot and In situ autoradiography demonstrated gene ablation was successful.