title: Presynaptic and postsynaptic mechanisms of a novel form of homosynaptic potentiation at aplysia sensory-motor neuron synapses.
abstract: Previous studies have shown that homosynaptic potentiation produced by rather mild tetanic stimulation (20 Hz, 2 sec) at Aplysia sensory-motor neuron synapses in isolated cell culture involves both presynaptic and postsynaptic Ca2+ (Bao et al., 1997). We have now investigated the sources of Ca2+ and some of its downstream targets. Although the potentiation lasts >30 min, it does not require Ca2+ influx through either NMDA receptor channels or L-type Ca2+ channels. Rather, the potentiation involves metabotropic receptors and intracellular Ca2+ release from both postsynaptic IP3-sensitive and presynaptic ryanodine-sensitive stores. In addition, it involves protein kinases, including both presynaptic and postsynaptic CamKII and probably MAP kinase. Finally, it does not require transsynaptic signaling by nitric oxide but it may involve AMPA receptor insertion. The potentiation, thus, shares components of the mechanisms of post-tetanic potentiation, NMDA- and mGluR-dependent long-term potentiation, and even long-term depression, but is not identical to any of them. These results are consistent with the more general idea that there is a molecular alphabet of basic components that can be combined in various ways to create novel as well as known types of plasticity.
authors.affiliation: Center for Neurobiology and Behavior, Columbia University, and New York State Psychiatric Institute, New York, New York 10032, USA.
authors.forename: Iksung
authors.initials: I
authors.lastname: Jin
authors.forename: Robert D
authors.initials: RD
authors.lastname: Hawkins
mesh_terms: D000818:Animals; D001048:Aplysia; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism / Q000502:physiology; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000502:physiology; D018920:Coculture Techniques; D053496:Inositol 1,4,5-Trisphosphate Receptors; D017136:Ion Transport; D017774:Long-Term Potentiation; D020935:MAP Kinase Signaling System; D009046:Motor Neurons / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D009473:Neuronal Plasticity; D009475:Neurons, Afferent / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology; D011494:Protein Kinases / Q000502:physiology; D018091:Receptors, AMPA / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D017661:Receptors, Presynaptic / Q000502:physiology; D019837:Ryanodine Receptor Calcium Release Channel / Q000502:physiology; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission
chemical_list: D015220:Calcium Channels; D053496:Inositol 1,4,5-Trisphosphate Receptors; D018091:Receptors, AMPA; D018160:Receptors, Cytoplasmic and Nuclear; D016194:Receptors, N-Methyl-D-Aspartate; D017661:Receptors, Presynaptic; D019837:Ryanodine Receptor Calcium Release Channel; D009569:Nitric Oxide; D011494:Protein Kinases; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D002118:Calcium