The use of gene deletion by homologous recombination to determine gene or p
rotein function has wide application in vertebrate neurobiology. An ideal c
omplement to gene deletion would be subsequent gene replacement to demonstr
ate re-acquisition of function. Here we used an adenoviral vector to replac
e the olfactory marker protein (OMP) gene in olfactory receptor neurons of
adult OMP-null mice and demonstrated the subsequent re-acquisition of funct
ion. Our results show that short-term expression of OMP restores the kineti
cs of electrophysiological responses of OMP-null mice to those of the contr
ol phenotype. This adenoviral-mediated rescue of the OMP-null phenotype is
consistent with involvement of OMP in olfactory transduction.