Our results on hippocampal long-term potentiation are considered in th
e context of Xia et al.'s hypothesis. Whereas the target article propo
ses presynaptic PKC involvement in adenylyl cyclase activation by phos
phorylation of neuromodulin, we suggest an additional postsynaptic rol
e involving RC3/neurogranin. Finally, we examine the possibility that
the adenylyl cyclase mutant mouse may display normal learning with a s
elective impairment of memory.