ABSTRACT
Mice from which the olfactory marker protein (OMP) gene has been deleted demonstrate a number of neurophysiologic and behavioral defects that suggest OMP is an important component in olfactory signal transduction and is critically involved in odor processing. Recently, the potential pleiotropic effects of gene deletion were addressed by adenoviral vector-mediated rescue of the neurophysiologic defects, in vivo. As a complement to this study, the authors used a recombinant adenoviral vector to transiently introduce OMP into olfactory sensory neurons of adult OMP-null mice and, using psychophysical methods, demonstrated the resulting reacquisition of behavioral function subsequent to gene replacement. The rescue of the OMP-null behavioral phenotype further supports the hypothesis that OMP is an important component in olfactory signal amplification and/or transduction processing.
