B6.129P2-P2rx3^tm1Ckn/J

Stock number: 003951
Product name: P2X₃-
Research areas: Sensorineural Research

Description

These P2rx3 knock-out mice exhibit a marked urinary bladder hyporeflexia along with reduced pain-related behavior in response to injection of ATP and formalin.

Detailed description

Mice that are homozygous null for the P2rx3 gene are viable, fertile, normal in size and do not display any gross physical abnormalities. A significantly decreased nociceptive response (hindpaw lifting, licking, biting) is observed in response to injection of ATP, and to a lesser extent formalin. Responses to noxious thermal and mechanical stimuli are similar to that seen in wild-type mice. Aged mice may develop cutaneous hypersensitivity. Mice also exhibit urinary bladder hyporeflexia, characterized by decreased micturition (urination) frequencies and increased bladder capacities. Whole-cell patch-clamp analysis indicates that homozygote null mice lose the rapidly desensitizing ATP-induced currents in dorsal root ganglion. This strain is suitable for use in studies examining afferent sensory pathways.

Development

A targeting vector containing loxP flanked neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt a region of the P2rx3 gene encoding intron 1. The construct was injected into 129P2/OlaHsd-derived E14-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. A chimeric animal was obtained. Mutant mice were then backcrossed to C57BL/6J mice for five generations using a speed congenic protocol.

Allele

Symbol: P2rx3^tm1Ckn
Name: targeted mutation 1, Debra A Cockayne
MGI accession ID: MGI:1934019
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: P2rx3
Marker name: purinergic receptor P2X, ligand-gated ion channel, 3
Chromosome: 2
Strain of origin: 129P2/OlaHsd
Molecular note: Exon 1 was replaced with a neomycin resistance gene via homologous recombination, thus deleting the translation initiation codon. Protein product was absent from dorsal root ganglion, spinal cord, and peripheral tissues of homozygous mutant animals as shown by immunohistochemistry.