Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. No gene product (protein) binding is detected in brain by autoradiographic analysis. SCN (suprachiasma nucleus) slices from homozygous mice do not exhibit suppression of neuronal firing in response to melatonin. In vitro, melatonin at higher concentrations causes phase shifts (~4hr phase advance) suggesting another receptor can influence SCN phase. Homozygous mice do not phase shift in response to melatonin injections. Overall homozygotes do not have obvious behavioral deficits, but detailed examination reveals that homozygotes have sensormotor deficits (impaired sensorimotor gating), acoustic startle/prepulse inhibition and increases in depressive-like behaviors (spend more time floating in the Porsolt test). These mice are on the C3H genetic background and carry the retinal degeneration allele Pde6brd1. This mutant mouse strain may be useful in studies of circadian rhythm and behavior.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
