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Sci. Signal., 12 August 2008
Vol. 1, Issue 32, p. ec292
[DOI: 10.1126/scisignal.132ec292]

EDITORS' CHOICE

Neuroscience Modulating Striatal Synapses

Peter Stern

Science, AAAS, Cambridge CB2 1LQ, UK

The role of dopamine in plasticity at glutamatergic synapses in the striatum is central to our understanding of basal ganglia functions and dopamine-dependent reward mechanisms. Long-term potentiation (LTP) and long-term depression (LTD) at these synapses are thought to be dependent on D1 and D2 dopamine receptors, respectively. However, the mechanisms of LTP and LTD in the striatum are controversial. Using brain slices from transgenic mice, Shen et al. show that LTP and LTD can occur in both D1- and D2-expressing neurons but with different molecular mechanisms. Dopaminergic modulation of plasticity is receptor and cell-type specific. The findings suggest that the control of bidirectional plasticity is not exerted through a monolithic mechanism, as previously asserted, but by cell-type-specific mechanisms depending on the subtype of dopamine receptor expressed.

W. Shen, M. Flajolet, P. Greengard, D. J. Surmeier, Dichotomous dopaminergic control of striatal synaptic plasticity. Science 321, 848-851 (2008). [Abstract] [Full Text]

Citation: P. Stern, Modulating Striatal Synapses. Sci. Signal. 1, ec292 (2008).

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