Nicotinic acetylcholine receptor-subunit mRNAs in the mouse superior cervical ganglion are regulated by development but not by deletion of distinct subunit genes

Mice with deletions of nicotinic ACh receptor (nAChR) subunit genes are valuable models for studying nAChR functions. We could previously show in the mouse superior cervical ganglion (SCG) that the absence of distinct subunits affects the functional properties of receptors. Here, we have addressed the question of whether deletions of the subunits α5, α7, or β2 are compensated at the mRNA level, monitored by reverse transcription and quantitative real-time polymerase chain reaction. Relative to our reference gene, α3, which is expressed in all SCG nAChRs, mRNA levels of β4 showed little change from birth until adult ages in intact ganglia of wild-type mice. In contrast, α4 declined sharply after birth and was barely detectable in adult animals. α5, α7, and β2 subunit message levels also declined, though more slowly and less completely than α4. The subunits α6 and β3 were detected by conventional polymerase chain reaction at very low levels, if at all, whereas α2 was never seen in any of our samples. The developmental profile of nAChR mRNA levels in the three knockout strains did not differ markedly from that of wild-type mice. Likewise, message levels of nAChR subunits were similar in cultures prepared from either wild-type or knockout animals. Our observations indicate a developmental regulation of nAChR subunit mRNAs in the SCG of mice after birth that was not affected by the three knockouts under investigation.