期刊
JOURNAL OF NEUROSCIENCE
卷 33, 期 22, 页码 9259-9272出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0237-13.2013
关键词
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资金
- National Institutes of Health (NIH) [DC007905, NS043277, HL058115, HL64937, DK072506, HL103455, AT006822]
- Hemsley Trust Grant from the U.S.-Israel Binational Science Foundation [BSF2011126]
- NIH Training Grant [F32DC011664]
Although it is well established that many glutamatergic neurons sequester Zn2+ within their synaptic vesicles, the physiological significance of synaptic Zn2+ remains poorly understood. In experiments performed in a Zn2+-enriched auditory brainstem nucleus-the dorsal cochlear nucleus-we discovered that synaptic Zn2+ and GPR39, a putative metabotropic Zn2+-sensing receptor (mZnR), are necessary for triggering the synthesis of the endocannabinoid 2-arachidonoylglycerol (2-AG). The postsynaptic production of 2-AG, in turn, inhibits presynaptic probability of neurotransmitter release, thus shaping synaptic strength and short-term synaptic plasticity. Zn2+-induced inhibition of transmitter release is absent in mutant mice that lack either vesicular Zn2+ or the mZnR. Moreover, mass spectrometry measurements of 2-AG levels reveal that Zn2+-mediated initiation of 2-AG synthesis is absent in mice lacking the mZnR. We reveal a previously unknown action of synaptic Zn2+:synaptic Zn2+ inhibits glutamate release by promoting 2-AG synthesis.
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