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The Journal of Neuroscience, May 9, 2007, 27(19):5260-5264; doi:10.1523/JNEUROSCI.0018-07.2007

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Brief Communications
Mechanisms for Synapse Specificity during Striatal Long-Term Depression

Sheela Singla, Anatol C. Kreitzer, and Robert C. Malenka

Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, California 94304

Correspondence should be addressed to Robert C. Malenka, Department of Psychiatry, Stanford Medical Center, 1201 Welch Road, Room P105, Palo Alto, CA 94304-5485. Email: malenka{at}stanford.edu

Endocannabinoid (eCB)-mediated forms of long-term synaptic plasticity occur in several brain regions, but much remains unknown about their basic properties and underlying mechanisms. Here, we present evidence that eCB-mediated long-term depression (eCB-LTD) at excitatory synapses on medium spiny neurons in the striatum requires presynaptic activity coincident with CB1 receptor activation. This dual requirement for CB1 activation and presynaptic activity is a mechanism by which eCB-LTD may be made synapse specific.

Key words: endocannabinoid; striatum; synaptic plasticity; basal ganglia; dopamine; LTD

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Received Jan. 3, 2007; revised April 10, 2007; accepted April 13, 2007.

Correspondence should be addressed to Robert C. Malenka, Department of Psychiatry, Stanford Medical Center, 1201 Welch Road, Room P105, Palo Alto, CA 94304-5485. Email: malenka{at}stanford.edu

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