NPY-Deficient mice
Introduction NEUROPEPTIDE Y (NPY), a 36-amino-acid transmitter distributed throughout the nervous system, is thought to function as a central stimulator of feeding behaviour. NPY has also been implicated in the modulation of mood, cerebrocortical excitability, hypothalamic–pituitary signalling, cardiovascular physiology and sympathetic function. Technology 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 or protein) is detected by Northern or Western blot analysis of brain or adrenal gland tissue. Beta-galactosidase activity assays and in situ hybridization demonstrate similar expression patterns for the lacZ gene and the endogenous wildtype gene. Spontaneous seizures are exhibited by some mice at age 6 to 8 weeks. Homozygous mice are susceptible to seizures induced by GABA antagonist treatment. Mutant mice have an increased sensitivity to leptin treatment which results in a greater initial reduction of food intake and weight loss when compared to wildtype mice. This mutant mouse strain may be useful in studies related to the role of neuropeptide Y in obesity. A targeting vector containing neomycin resistance, thymidine kinase and lacZ reporter genes was used to disrupt exon 2 of the targeted gene. The construct was electroporated into 129S6/SvEvBrd-Hprt+ derived AB1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Related Publication(s)
Nature 1996, 381, 415 – 418
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