Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. In heterozygote crosses, the number of homozygous progeny born (15%) does not reach the expected Mendelian ratio indicating low survival of homozygous embryos. No gene product (mRNA or alpha and delta isoform proteins) is detected. The beta isoform gene product is up regulated. cAMP response element modulation protein expression is up regulated 2- to 3-fold. Although fear conditioning and Morris water maze testing demonstrate that homozygous mice have normal learning and short-term memory, long-term memory for cued and contextual conditioning is disrupted. Electrophysiological analysis of the hippocampus of mutant mice reveals abnormal long-term potentiation, which decays to baseline within 90 minutes, whereas wildtype controls display no decay. The long-term memory deficit exhibited by mutant mice can be overcome by additional spaced (10-60 minutes between trials) training. Homozygous mutant mice treated with chronic morphine administration exhibit reduced opiate tolerance and diminished morphine withdrawal. This mutant mouse strain may be useful in studies related to the molecular mechanisms of long-term memory and in studies related to the chronic effects of drug abuse.

These <i> Creb1</i> knock-out mice exhibit long-term memory deficit.

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