title: Contribution of PKC to the maintenance of 5-HT-induced short-term facilitation at sensorimotor synapses of Aplysia.
abstract: Aplysia sensorimotor synapses provide a useful model system for analyzing molecular processes that contribute to heterosynaptic plasticity. For example, previous studies demonstrated that multiple kinase cascades contribute to serotonin (5-HT)-induced short-term synaptic facilitation (STF), including protein kinase A (PKA) and protein kinase C (PKC). Moreover, the contribution of each kinase is believed to depend on the state of the synapse (e.g., depressed or nondepressed) and the time after application of 5-HT. Here, a previously unappreciated role for PKC-dependent processes was revealed to underlie the maintenance of STF at relatively nondepressed synapses. This PKC dependence was revealed when the synapse was stimulated repeatedly after application of 5-HT. The contributions of the PKA and PKC pathways were examined by blocking adenylyl cyclase-coupled 5-HT receptors with methiothepin and by blocking PKC with chelerythrine. STF was assessed 20 s after 5-HT application. The effects of PKC were consistent with enhanced mobilization of transmitter, as assessed by application of hypertonic sucrose solutions to measure the readily releasable pool of vesicles and recovery of the readily releasable pool after depletion. A computational model of transmitter release demonstrated that a PKC-dependent mobilization process was sufficient to explain the maintenance of STF at nondepressed synapses and the facilitation of depressed synapses.
authors.affiliation: Department of Neurobiology and Anatomy, The University of Texas Medical School at Houston, Houston, Texas.
authors.forename: Lian
authors.initials: L
authors.lastname: Zhou
authors.affiliation: Department of Neurobiology and Anatomy, The University of Texas Medical School at Houston, Houston, Texas.
authors.forename: Douglas A
authors.initials: DA
authors.lastname: Baxter
authors.affiliation: Department of Neurobiology and Anatomy, The University of Texas Medical School at Houston, Houston, Texas John.H.Byrne@uth.tmc.edu.
authors.forename: John H
authors.initials: JH
authors.lastname: Byrne
mesh_terms: D000818:Animals; D001048:Aplysia; D003198:Computer Simulation; D004558:Electric Stimulation; D019706:Excitatory Postsynaptic Potentials; D008959:Models, Neurological; D009473:Neuronal Plasticity; D011493:Protein Kinase C / Q000378:metabolism*; D012701:Serotonin / Q000494:pharmacology / Q000502:physiology*; D013569:Synapses / Q000187:drug effects / Q000502:physiology*
chemical_list: D012701:Serotonin; D011493:Protein Kinase C
keywords: computational model; heterosynaptic facilitation; homosynaptic depression; sensorimotor synapses; synaptic plasticity; transmitter mobilization