期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2010
卷号：107
期号：35
页码：15607-15612
DOI：10.1073/pnas.1004451107
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Calmodulin (CaM)-sensitive adenylyl cyclase (AC) in sensory neurons (SNs) in Aplysia has been proposed as a molecular coincidence detector during conditioning. We identified four putative ACs in Aplysia CNS. CaM binds to a sequence in the C1b region of AC-AplA that resembles the CaM-binding sequence in the C1b region of AC1 in mammals. Recombinant AC-AplA was stimulated by Ca2+/CaM. AC-AplC is most similar to the Ca2+-inhibited AC5 and AC6 in mammals. Recombinant AC-AplC was directly inhibited by Ca2+, independent of CaM. AC-AplA and AC-AplC are expressed in SNs, whereas AC-AplB and AC-AplD are not. Knockdown of AC-AplA demonstrated that serotonin stimulation of cAMP-dependent plasticity in SNs is predominantly mediated by this CaM-sensitive AC. We propose that the coexpression of a Ca2+-inhibited AC in SNs, together with a Ca2+/CaM-stimulated AC, would enhance the associative requirement for coincident Ca2+ influx and serotonin for effective stimulation of cAMP levels and initiation of plasticity mediated by AC-AplA.
