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The Journal of Neuroscience, December 15, 1998, 18(24):10310-10319
Use-Dependent Decline of Paired-Pulse Facilitation at Aplysia Sensory Neuron Synapses Suggests a Distinct Vesicle Pool or Release Mechanism
Xue-Ying Jiang and Thomas W. Abrams Departments of Pharmacology and Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland 21201-1559
We have characterized paired-pulse facilitation at Aplysia sensory neuron-to-motoneuron synapses. This simple form of very short-term synaptic plasticity displayed an unusual feature: it decreased dramatically with repeated testing. Synaptic depression at these synapses and this use-dependent decrease in paired-pulse facilitation occurred independently of each other. Paired-pulse facilitation was inversely correlated with the size of the initial synaptic connection and was absent at stronger synapses. The use-dependent decrease in paired-pulse facilitation occurred at the same rate at large synapses as at small synapses, although the initial paired-pulse facilitation at large synapses was substantially smaller. Rates of synaptic depression were also independent of initial synaptic strength. Paired-pulse facilitation was blocked by presynaptic EGTA injection, but not by postsynaptic EGTA or BAPTA injection. These results indicate that presynaptic Ca2+ influx plays a critical role in paired-pulse facilitation. However, the persistence of the decrease in paired-pulse facilitation for longer than 15 min suggests that Ca2+ from the first paired action potential produces facilitation via a modulatory mechanism rather than by summating with Ca2+ influx during the second paired action potential in activating the Ca2+ binding sites that initiate exocytosis. This modulatory mechanism may not involve protein phosphorylation because paired-pulse facilitation was unaffected by the protein kinase inhibitors H7 and KN-62. These findings further suggest that release by the second paired action potential occurs at sites distinct from those that mediate release by the first action potential.
Key words: synaptic plasticity; facilitation; synaptic depression; Aplysia; paired-pulse facilitation; calcium; phosphorylation
Copyright © 1998 Society for Neuroscience 0270-6474/98/182410310-10$05.00/0
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