Pioneering work suggests that a synaptic active zone protein, RIM1, regulates both short- and long-term glutamatergic presynaptic plasticity at certain synapses. In short-term plasticity, RIM1 accelerates the priming of synaptic vesicles for fusion; by contrast, in long-term potentiation of mossy fiber synapses in the hippocampal CA3 region, phosphorylated RIM1 acts through an unknown molecular pathway to enhance release of the excitatory neurotransmitter glutamate.
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