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The Journal of Neuroscience, May 1, 1998, 18(9):3147-3157

Calcium-Dependent Regulation of Rab3 in Short-Term Plasticity

Frédéric Doussau¹, Aude Clabecq², Jean-Pierre Henry², François Darchen², and Bernard Poulain¹

¹ Laboratoire de Neurobiologie Cellulaire, UPR 9009, Centre National de la Recherche Scientifique, F-67084 Strasbourg Cedex, France, and ² Service de Neurobiologie Physico-Chimique, Centre National de la Recherche Scientifique, ERS 575, Institut de Biologie Physico-Chimique, F-75005 Paris, France

The Rab3 proteins are monomeric GTP-binding proteins associated with secretory vesicles. In their active GTP-bound state, Rab3 proteins are involved in the regulation of hormone secretion and neurotransmitter release. This action is thought to involve specific effectors, including two Ca²⁺-binding proteins, Rabphilin and Rim. Rab3 acts late in the exocytotic process, in a cell domain in which the intracellular Ca²⁺ concentration is susceptible to rapid changes. Therefore, we examined the possible Ca²⁺-dependency of the regulatory action of GTP-bound Rab3 and wild-type Rab3 on neuroexocytosis at identified cholinergic synapses in Aplysia californica. The effects of recombinant GTPase-deficient Aplysia-Rab3 (apRab3-Q80L) or wild-type apRab3 were studied on evoked acetylcholine release. Intraneuronal application of apRab3-Q80L in identified neurons of the buccal ganglion of Aplysia led to inhibition of neurotransmission; wild-type apRab3 was less effective. Intracellular chelation of Ca²⁺ ions by EGTA greatly potentiated the inhibitory action of apRab3-Q80L. Train and paired-pulse facilitation, two Ca²⁺-dependent forms of short-term plasticity induced by a rise in intraterminal Ca²⁺ concentration, were increased after injection of apRab3-Q80L. This result suggests that the inhibition exerted by GTP-bound Rab3 on neuroexocytosis is reduced during transient augmentations of intracellular Ca²⁺ concentration. Therefore, a Ca²⁺-dependent modulation of GTP-bound Rab3 function may contribute to short-term plasticity.

Key words: Aplysia; synapse; synaptic vesicle exocytosis; neurotransmitter release mechanism; Rab3; facilitation; post-tetanic potentiation; synaptic plasticity

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Copyright © 1998 Society for Neuroscience  0270-6474/98/1893147-11$05.00/0

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