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The Journal of Neuroscience, August 13, 2003, 23(19):7288-7297

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Presynaptic and Postsynaptic Mechanisms of a Novel Form of Homosynaptic Potentiation at Aplysia Sensory-Motor Neuron Synapses

Iksung Jin¹ and Robert D. Hawkins^1,2

¹Center for Neurobiology and Behavior, Columbia University, and ²New York State Psychiatric Institute, New York, New York 10032

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.

Key words: Aplysia; potentiation; presynaptic; postsynaptic; Ca²⁺ stores; CamKII

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Received Apr. 15, 2003; revised Jun. 18, 2003; accepted Jun. 18, 2003.

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