Author
Listed:
- Pablo E. Castillo
(Departments of Cellular and Molecular Pharmacology
Facultad de Medicina)
- Roger Janz
(The University of Texas Southwestern Medical Center)
- Thomas C. Sdhof
(The University of Texas Southwestern Medical Center)
- Thanos Tzounopoulos
(Departments of Psychiatry and San Francisco)
- Robert C. Malenka
(Departments of Psychiatry and San Francisco
University of California)
- Roger A. Nicoll
(Departments of Cellular and Molecular Pharmacology
University of California)
Abstract
Repetitive activation of excitatory synapses in the central nervous system results in a long-lasting increase in synaptic transmission called long-term potentiation (LTP). It is generally believed that this synaptic plasticity may underlie certain forms of learning and memory. LTP at most synapses involves the activation of the NMDA (N-methyl-d-aspartate) subtype of glutamate receptor, but LTP at hippocampal mossy fibre synapses is independent of NMDA receptors and has a component that is induced and expressed presynaptically1. It appears to be triggered by a rise in presynaptic Ca2+(refs 2, 3), and requires the activation of protein kinase A4,5,6, which leads to an increased release of glutamate3,7,8,9,10. Agreat deal is known about the biochemical steps involved in the vesicular release of transmitter11,12,13, but none of these steps has been directly implicated in long-term synaptic plasticity. Here we show that, although a variety of short-term plasticities are normal, LTP at mossy fibre synapses is abolished in mice lacking the synaptic vesicle protein Rab3A.
Suggested Citation
Pablo E. Castillo & Roger Janz & Thomas C. Sdhof & Thanos Tzounopoulos & Robert C. Malenka & Roger A. Nicoll, 1997.
"Rab3A is essential for mossy fibre long-term potentiation in the hippocampus,"
Nature, Nature, vol. 388(6642), pages 590-593, August.
Handle:
RePEc:nat:nature:v:388:y:1997:i:6642:d:10.1038_41574
DOI: 10.1038/41574
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