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 or protein) is detected by RT-PCR of intestinal tissue or Western blot analysis of dorsal root and trigeminal ganglia. No immunoreactive staining was detected in ileum by immunohistochemical analysis. Myenteric neurons exhibit altered intracellular electrophysiological action potentials. Fast excitatory postsynaptic potentials (fEPSPs) from mutant S neurons (myenteric plexus interneurons and motorneurons) are inhibited by the nicotinic cholinergic receptor antagonist, mecamylamine. ATP-induced depolarization of isolated mutant S neurons is abolished. Peristalsis is impaired in the ileum. Mutant mice ventilatory response to hypoxia is diminished, as determined by in vitro carotid sinus nerve preparation. ATP and ATP analog (alpha,beta-methyleneATP) elicits a faster discharge (afferent activity) in mutant sinus nerves. This mutant mouse strain may be useful in studies related to pain and peripheral nerve hypersensitivity, and sensory perception.

Myenteric neurons  from these <i> P2rx2</i> knock-out mice exhibit altered intracellular electrophysiological action potentials. Peristalsis in mutant mice is impaired in the ileum, and  ventilatory response to hypoxia is diminished.

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