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Sci. STKE, 15 April 2003
Vol. 2003, Issue 178, p. tw146
[DOI: 10.1126/stke.2003.178.tw146]


SYNAPTIC PLASTICITY Multiple Ways to Enhance Neurotransmitter Release

Neurotransmitter release is dynamic and is influenced by the prior history of neuronal firing and the subsequent entry of Ca2+ into the nerve terminal. The precise mechanisms linking neuronal activity to various short-term processes that modulate neurotransmitter release and thus synaptic efficacy, however, have remained unclear. Two papers shed light on different aspects of Ca2+-dependent regulation of short-term synaptic plasticity. Chi et al. investigated use-dependent modulation of synaptic vesicle mobilization through synapsin I, which regulates vesicle availability through phosphorylation-dependent association with the cytoskeleton. They discovered regulation through different signaling pathways at different frequencies of stimulation. The authors used confocal microscopy to monitor synaptic vesicles simultaneously with synapsin I in cultured rat hippocampal neurons and found that synapsin I dispersal correlated with vesicle turnover across a range of stimulation frequencies. Immunofluorescent analysis together with measurements of vesicle turnover and the dispersal of synapsin I mutants with alterations to their phosphorylation sites indicated that sites phosphorylated by Ca2+-calmodulin-dependent protein kinase II regulated mobilization at low stimulation frequencies. In contrast, frequency-dependent phosphorylation and dephosphorylation of sites phosphorylated by mitogen-activated protein kinase and dephosphorylated by calcineurin-modulated mobilization across a range of frequencies. Thus, synapsin I appeared to modulate vesicle availability in response to activation of distinct signaling pathways at different stimulation frequencies. Blatow et al. investigated the effects of endogenous and exogenous Ca2+ buffers on paired-pulse facilitation, the briefest form of use-dependent enhancement of synaptic efficacy, in synaptically connected neurons in mouse neocortical and hippocampal slices. By using a combination of conditions-including washout of endogenous buffers, mutant mice lacking the endogenous buffer calbindin-D28k (CB), and loading with exogenous buffers or CB-the authors implicated local saturation of CB in paired-pulse facilitation in CB-containing nerve terminals.

P. Chi, P. Greengard, T. A. Ryan, Synaptic vesicle mobilization is regulated by distinct synapsin I phosphorylation pathways at different frequencies. Neuron 38, 69-78 (2003). [Online Journal]

M. Blatow, A. Caputi, N. Burnashev, H. Monyer, A. Rozov, Ca2+ buffer saturation underlies paired pulse facilitation in calbindin-D28k-containing terminals. Neuron 38, 79-88 (2003). [Online Journal]

Citation: Multiple Ways to Enhance Neurotransmitter Release. Sci. STKE 2003, tw146 (2003).

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