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The Journal of Neuroscience, November 15, 2006, 26(46):11811-11820; doi:10.1523/JNEUROSCI.3196-06.2006

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Cellular/Molecular
The Role of Protein Synthesis in Striatal Long-Term Depression

Henry H. Yin, Margaret I. Davis, Jennifer A. Ronesi, and David M. Lovinger

Section on Synaptic Pharmacology, Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland 20892

Correspondence should be addressed to David M. Lovinger, National Institute on Alcohol Abuse and Alcoholism–National Institutes of Health, 5625 Fishers Lane, TS-13, Bethesda, MD 20892. Email: lovindav{at}willco.niaaa.nih.gov

Long-term depression (LTD) at the corticostriatal synapse is postsynaptically induced but presynaptically expressed, the depression being a result of retrograde endocannabinoid signaling that activates presynaptic cannabinoid CB₁ receptors and reduces the probability of glutamate release. To study the role of protein synthesis in striatal LTD, we used a striatum-only preparation in which the presynaptic cell body is cut off, leaving intact only its axons, whose terminals synapse on medium spiny neurons. LTD (duration >150 min) was induced in this preparation, thus providing evidence that transcription in the presynaptic cell nucleus is not necessary for this form of plasticity. The maintenance of striatal LTD, however, was blocked by bath application of protein translation inhibitors but not by the same inhibitors loaded into the postsynaptic cell. These results suggest that local translation is critical for the expression of striatal LTD, distinguishing this form of mammalian synaptic plasticity from other forms that require postsynaptic protein synthesis. Possible roles of axonal or glial translation in striatal LTD are considered.

Key words: long-term depression; protein synthesis; cycloheximide; translation; striatum; endocannabinoid; plasticity

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Received July 26, 2006; revised Oct. 3, 2006; accepted Oct. 4, 2006.

Correspondence should be addressed to David M. Lovinger, National Institute on Alcohol Abuse and Alcoholism–National Institutes of Health, 5625 Fishers Lane, TS-13, Bethesda, MD 20892. Email: lovindav{at}willco.niaaa.nih.gov

This article has been cited by other articles:

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				L. Adermark and D. M. Lovinger Retrograde endocannabinoid signaling at striatal synapses requires a regulated postsynaptic release step PNAS, December 18, 2007; 104(51): 20564 - 20569. [Abstract] [Full Text] [PDF]

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