期刊
NEURON
卷 67, 期 1, 页码 116-128出版社
CELL PRESS
DOI: 10.1016/j.neuron.2010.05.030
关键词
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资金
- Deutsche Forschungsgemeinschaft [DI 702/6-1]
- Italian Institute of Technology
- Wellcome Trust
- Medical Research Council UK
- New Jersey Commission for Spinal Cord Research
- MRC [G0900613, G0802216] Funding Source: UKRI
- Medical Research Council [G0900613, G0802216] Funding Source: researchfish
Although the extracellular matrix plays an important role in regulating use-dependent synaptic plasticity, the underlying molecular mechanisms are poorly understood. Here we examined the synaptic function of hyaluronic acid (HA), a major component of the extracellular matrix. Enzymatic removal of HA with hyaluronidase reduced nifedipine-sensitive whole-cell Ca2+ currents, decreased Ca2+ transients mediated by L-type voltage-dependent Ca2+ channels (L-VDCCs) in postsynaptic dendritic shafts and spines, and abolished an L-VDCC-dependent component of long-term potentiation (LTP) at the CA3-CA1 synapses in the hippocampus. Adding exogenous HA, either by bath perfusion or via local delivery near recorded synapses, completely rescued this LTP component. In a heterologous expression system, exogenous HA rapidly increased currents mediated by Ca(v)1.2, but not Ca(v)1.3, subunit-containing L-VDCCs, whereas intrahippocampal injection of hyaluronidase impaired contextual fear conditioning. Our observations unveil a previously unrecognized mechanism by which the perisynaptic extracellular matrix influences use-dependent synaptic plasticity through regulation of dendritic Ca2+ channels.
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