Abstract

It has been suggested that type I adenylyl cyclase may play a unique role in long-term potentiation, due to both unique regulatory properties as well as a specialized distribution within the mammalian brain. This would allow an integration of the signals wrought by increased intracellular calcium with those conveyed into the cellular milieu via increased cAMP. These results are discussed in the context of changes in cellular structure, because of changing interactions between G proteins and cytoskeletal components, which might be expected to accompany chronic synaptic activation