Serotonin stimulation of cAMP-dependent plasticity in Aplysia sensory neurons is mediated by calmodulin-sensitive adenylyl cyclase |
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| Authors: | Allison H. Lin Jonathan E. Cohen Qin Wan Katelyn Niu Pragya Shrestha Steven L. Bernstein Thomas W. Abrams |
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| Affiliation: | aDepartment of Pharmacology.;bProgram in Neuroscience, and;cDepartment of Ophthalmology, University of Maryland School of Medicine, Baltimore, MD 21201-1559 |
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| Abstract: | 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. |
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| Keywords: | coincidence detector associative learning synaptic plasticity classical conditioning calcium |
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