title: Rapid increase in clusters of synaptophysin at onset of homosynaptic potentiation in Aplysia.
abstract: Imaging studies have shown that even the earliest phases of long-term plasticity are accompanied by the rapid recruitment of synaptic components, which generally requires actin polymerization and may be one of the first steps in a program that can lead to the formation of new stable synapses during late-phase plasticity. However, most of those results come from studies of long-term potentiation in rodent hippocampus and might not generalize to other forms of synaptic plasticity or plasticity in other brain areas and species. For example, recruitment of presynaptic proteins during long-term facilitation by 5HT in Aplysia is delayed for several hours, suggesting that whereas activity-dependent forms of plasticity, such as long-term potentiation, involve rapid recruitment of presynaptic proteins, neuromodulatory forms of plasticity, such as facilitation by 5HT, involve more delayed recruitment. To begin to explore this hypothesis, we examined an activity-dependent form of plasticity, homosynaptic potentiation produced by tetanic stimulation of the presynaptic neuron in Aplysia. We found that homosynaptic potentiation involves presynaptic but not postsynaptic actin and a rapid (under 10 min) increase in the number of clusters of the presynaptic vesicle-associated protein synaptophysin. These results indicate that rapid recruitment of synaptic components is not limited to hippocampal potentiation and support the hypothesis that activity-dependent types of plasticity involve rapid recruitment of presynaptic proteins, whereas neuromodulatory types of plasticity involve more delayed recruitment.
authors.affiliation: Department of Neuroscience, Columbia University, New York, NY 10032, USA.
authors.forename: Iksung
authors.initials: I
authors.lastname: Jin
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Udo
authors.forename: Robert D
authors.initials: RD
authors.lastname: Hawkins
mesh_terms: D000199:Actins / Q000502:physiology; D000818:Animals; D030801:Animals, Genetically Modified; D001048:Aplysia / Q000235:genetics / Q000502:physiology*; D055724:Electrophysiological Phenomena; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D017774:Long-Term Potentiation / Q000502:physiology; D009046:Motor Neurons / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D017729:Presynaptic Terminals / Q000502:physiology; D011993:Recombinant Fusion Proteins / Q000235:genetics / Q000378:metabolism; D011984:Sensory Receptor Cells / Q000502:physiology; D012701:Serotonin / Q000502:physiology; D013569:Synapses / Q000502:physiology*; D016708:Synaptophysin / Q000235:genetics / Q000502:physiology*
chemical_list: D000199:Actins; D011993:Recombinant Fusion Proteins; D016708:Synaptophysin; D049452:Green Fluorescent Proteins; D012701:Serotonin