Abstract
Alterations in the amount of released neurotransmitter are responsible for multiple forms of short- and long-term synaptic plasticity. At many synapses it is unclear if this presynaptic plasticity is mediated by direct regulation of Ca2+ current through presynaptic channels or through other targets that act more indirectly on the release apparatus. The Zucker laboratory has revisited this question in its investigations of long-term facilitation (LTF) of neurotransmitter release at the crayfish neuromuscular junction. Their surprising results, recently published in The Journal of Physiology (Minami et al. 2007), are likely to have wider implications for studies addressing regulation of presynaptic Ca2+ signalling during synaptic plasticity.
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